Sequentially programmed magnetic field therapeutic system (spmf)

ABSTRACT

A comprehensive system for inducing cellular regeneration and/or degeneration processes and methods of treatment based on such processes through generating and applying a sequentially programmed magnetic field (SPMF) to the area to be treated. In the case of regeneration and degeneration of cells, the pulsing frequencies are in the range of about 0.1 to about 2000 Hz based on the indication of the disease type which was determined by either the patient&#39;s MRI, CT, Ultrasound or other diagnostic information. Methods for treating diseases or conditions that will benefit from regeneration and/or degeneration of cells. For example, methods for treating cancer, arthritis, neuro degeneration conditions, such as the age-related progressive loss of nerve cells, Alzheimer&#39;s, Parkinson&#39;s, ALS, and Huntington&#39;s disease, retinal degeneration, and other damage to sensory systems (e.g., visual, auditory, somatosensory), in stroke, head and spinal trauma, epilepsy, in drug and alcohol abuse, in infectious diseases, in exposure to industrial and environmental toxicants, and, perhaps, in mental disorders and chronic pain. Methods for treating non-healing fractures and other bone disorders are also disclosed.

This application claims priority to Indian Provisional Specification no.184/MUM/2009, entitled AN APPARATUS FOR INDUCING MAGNETIC RESONANCE INBIOLOGICAL TISSUES, filed on Jan. 30, 2009 and to U.S. ProvisionalPatent Application Ser. No. 61/285,712, entitled SEQUENTIALLY PROGRAMMEDMAGNETIC FIELD THERAPEUTIC SYSTEM (SPMF), filed on Dec. 11, 2009. Theentire content of each application is hereby incorporated by referencefor any purpose.

TECHNOLOGY FIELD

The invention relates to systems for generating and inducingsequentially programmed magnetic fields (SPMFs) in biological tissue(s)and methods for inducing cellular regeneration and/or degenerationprocesses and methods of treatment based on such processes using such asystem. More particularly, the invention relates to a SPMF therapeuticsystem and method for the regeneration or degeneration of biologicaltissue(s). More particularly, it relates to an apparatus or system forgenerating and applying SPMFs to biological tissue(s) which resonatestherein.

BACKGROUND

It is known that electromagnetic fields of certain frequency ranges andintensities are indigenous to living tissues and it has been found thatinciting the inherent resonance by exogenous treatment usingelectromagnetic fields [EMF], electric fields, and magnetic fields caninduce cellular regeneration and degeneration processes. EMF in a rangefrom 0.1-150 Hz have been reported to stimulate bone cells. It has alsobeen reported that bone resorption that normally parallels disuse can beprevented or even reversed by the exogenous induction of electricfields. Electromagnetic fields below 10 microV/cm, when induced atfrequencies between 50 and 150 Hz for 1 h/day, are sufficient tomaintain bone mass even in the absence of function. Reducing thefrequency to 15 Hz makes the field extremely osteogenic. Thisfrequency-specific sinusoidal field initiated more new bone formationthan a more complex pulsed electromagnetic field (PEMF), though inducingonly 0.1% of the electrical energy of the PEMF.

In Yuri Gagarin's historic flight into space, he returned in nearcritical condition after only one hour and forty eight minutes in space.Clearly there was some vital element missing in space that we receive onearth. Yuri had plenty of food, water, and oxygen and since the flightwas less than 2 hours he really only needed oxygen. The critical missingelement appears to be PEMF—Pulsed Electromagnetic Fields. Since thatfirst flight, pulsed magnetic devices have been used in every space suitand space station. Further studies have been done on earth (zero fieldstudies) with both laboratory animals and human subjects. In a matter ofhours without exposure to healthy PEMF's, cell metabolism begins tobreak down causing bone loss, muscle weakness, depressed metabolism,disorientation and depression.

A range of PEMF machines have been introduced in the market. PEMFtherapy has been reported to decrease pain, improve sleep, enhancecirculation, regenerate nerves, help in healing of wounds, enhanceimmunity and improve bone density.

An area of immense interest has been the use of magnetic stimulation inrehabilitating injured or paralyzed muscle groups. Magnetic stimulationof the heart has been considered to be superior to CPR or electricalstimulation, because both of those methods apply gross stimulation tothe entire heart all at once. A magnetic stimulator can be used as anexternal pacer to stimulate each chamber of the heart separately in theproper sequence. Another area in which magnetic stimulation is provingeffective is treatment of the spine. The spinal cord is difficult toaccess directly because vertebrae surround it. Magnetic stimulation maybe used to block the transmission of pain via nerves in the back, e.g.,those responsible for lower back pain. Magnetic stimulation also hasproven effective in stimulating regions of the brain thereby providing anumber of treatment options including several classes of anti-depressantmedications (Sari's, MAI's and tricyclics), lithium, andelectroconvulsive therapy (ECT). Recently, repetitive transcranialmagnetic stimulation (rTMS) has also been shown to have significantanti-depressant effects for patients that do not respond to thetraditional methods. The membranes are depolarized by the induction ofsmall electric fields in excess of 1 V/cm that are the result of arapidly changing magnetic field applied non-invasively.

The use of electromagnetic fields (EMFs) for healing has been known fromtime immemorial. Even many centuries back, simple magnets were used forregenerative purposes. It is only in the last 50 years that specific useof electromagnetic fields has been clearly defined to aid in orfacilitate biological tissue regeneration or degeneration. Much researchhas gone into this use of electromagnetic fields. In the last 50 yearsresearch has established a scientific basis for use of electromagneticdevices in the treatment of illness, although many applications have yetto be specific enough to achieve the desired changes.

Each tissue in the body is made of cells and a cell is the smallestdistinct entity of that particular type of tissue. The cell has aspecific cell membrane and the cell membrane is a dividing structurethat maintains biochemically distinct compartments between the insideand outside of the cell. The inside is the intracellular compartment andthe outside is the extracellular space, as described by Marieb in 1998.In order to maintain a balance there is a free exchange of electrolytes,water, sodium and potassium constantly through the intracellular andextracellular compartments. The passage of these electrically chargedions will create flow of electrical currents through the membrane. Theseions in turn affect the metabolism of the cell and potential of the cellmembrane. The normal cell membrane potential is about −70 to −90 mV. Alot of research has been done on how cell membrane potential is the keyto maintain cell activity and the behavior of the cell itself. ClarenceCone et. al. from 1970 was responsible for publication of majority ofscientific papers on this entity. The lipid structure of the cellmembrane makes it relatively impermeable to the transfer of the ions andtherefore, these ions pass through ion channels. The ions channelscontain aqueous pores that connect the inside of the cell to theextracellular space. These are open and shut based on a variety ofsignals. Dr. Steve Haltiwanger has described in his thesis on the use ofelectrotherapy for diseases on how to build up of differentconcentration of mineral ions and endow cell membrane with electricalproperty of capacitance. Capacitors are well known electrical componentsthat are composed of two conducting sheets of metal plates separated bythin layer of insulating material. The membrane of the cell organellethat have mitochondria in animals and the chloroplast in plants act asbiological capacitors and they have the capacity to accumulate and storecharge and hence energy can be given up when needed. A cell or a humanbody is coupled to its electric field in proportion to its capacitancesuch that the greater the frequency of the electric field, the greaterthe current flow of the cell for the body. For soft tissue low frequencynatural or applied electric field current will create current that areconducted primarily along the surface of the cell. This has beendescribed by Adey et. al. in 1993. When high frequency fields areapplied with external signal generators such as micro current devices,magnetic pulses or the plasma tubes or Rife devices, electrical chargingof the cell membrane occurs causing an increase in cell membranecapacitance and increased conduction of current through the cellmembrane. This is distinctly described by Haltiwanger also in 2003. Thismeans that the devices that generate low frequency current will havedifferent biological effects and the device that generates highfrequency can have different biological effect. In summary, increase incell membrane capacitances would change cell membrane permeability andcould cause significant changes in cell behavior.

Scientific research has proven that cells are electro magnetic in natureand they generate their own electro magnetic fields and are also capableof harnessing external electro magnetic energy in the right wave lengthand strength to communicate control and drive metabolic functions asdescribed by Adey in 1988 and 1993 as also by Becker in 1990. Theapplication of a varying magnetic flux to the area of the body willinduce an electric field along the perimeters of the area. This isaccording to the basic laws of electromagnetism. When varying magneticfields are applied to human tissues that contain free or chargedcarriers these charge carriers are accelerated by the electric fieldthereby generating eddy currents. The induced electric field or thegenerated current depends on the rate of change of the magnetic field.Time varying magnetic fields that induce cellgrowth acceleration, enzymeactivation and changes in membrane in metabolism have been describedearlier by Enforte in 1990. It is well recognized that electricalcurrents and magnetic fields are continuously produced in the body atall times. For example in the ECG—the Cardiologist measure theelectrical currents of the beating heart or in the EEG—the Neurologistmeasure the electrical activity of the brain, or in the EMG—theNeurologist measure the activity of the muscle and the nerve. Likewisewhole lot of other parameters that are related to this can be measured.Electricity in the body comes from the food that we eat and the air thatwe breathe. Lester Brown in 1999 described energy from enzyme catalysedchemical reaction which involves oxidation of fats, proteins andcarbohydrates. Cells can produce energy by oxidation, dependent aerobicenzyme particles and by less efficient fermentation process.

In regeneration, in normal people, for example, when weight is put onthe knees, the cartilage gets compressed and this itself is the stimulusfor the regeneration to start and there is forced efflux of hydrogenprotons causing changes in the cell membrane potential. This capacity islost in the osteoarthritic patient. However, by selectively alteringthis cell membrane potential by use of time varying electromagneticfields which are tuned to this specific resonating frequency one canre-induce this change into the cell at rest.

The use of electromagnetic fields in cancer therapy has been fairlysummarized by Marc Neveu PhD in his recent article on Explore Volume 12Nov. 4, 2003 wherein he has likened the DNA to act as the computer'sbinary code that runs various programs and the nucleus to the hard disk.Imagine the DNA mutations in cancer cells are like software problems orlike virus in system conflicts. An increase of software errors likemutations increase chaos in the system and slows down the computer'soverall performance. Actually cancer cells have many mutations in theDNA sequence that regulate the cell growth and can get stuck being onmode. As an example we can try to debug the program or the other way toget the computer work again is to reboot. So electromagnetic therapyusing electromagnetic waves having very specific frequency to retune tocellular programs can restore this programs and restore optimal celloperation. Normal cells restart following magnetic resonance therapywithout a problem because their DNA that is software normal. Howevercancer cells try to reboot, the multiple defect in the DNA as themutation, chromosome aberrations and viruses prevent restart which wouldcause tumor cells to stop growing or start the induction of thepro-apoptotic cycle and go into apoptosis. The frequency is essentiallythe number of time the electromagnetic waves repeats per second. Acomplete sinusoidal wave looks like the repetition of the letter S whichis sleeping. The frequency is directly proportional to the energy of asingle photon which means the higher the frequency, the higher theenergy. Low frequency energy waves carry less energy and have lesspenetrability. Every animate or living structure has a certain naturalinnate or resonating frequency and it applies to all levels fromorganisms to subatomic particles. When two objects having similar ornatural frequency come together, they interact without touching. Forexample when soldiers march in step on a bridge, the bridge can collapsedue to the resonance that is caused. On the other side, a soprano,singing with a high note can shatter its glass because it coincides withthe natural frequency of the glass. The atoms in the glass vibrate sostrongly because they are resonating with that frequency and they cannothold it together so they shatter. Cancer is the end result of a seriesof genetic alterations that modify the control of promoting (oncogenes)or inhibit (suppressor gene) cell proliferation. Conventionallychemotherapy and radiation employ nonspecific toxic effects to inhibitthe proliferation of both normal and tumor cells they are aimed at cellswhich are proliferating very rapidly and they have very significant sideeffects. The co-ordination between cell membrane potential and cancercell proliferation has been known for decades, one of the pioneers ofthis is Dr. Clarence Cone who in 1970 authored a classic paper. Directmeasurements have shown that there is 6-7 times higher conductance intumors compared to normal tissue. The electrical changes occur becauseof rapid proliferating and transformed cells have lower membranepotential when compared to normal cells. The cancer cells havetransmembrane potential which is about 20-30 mv which is much reduced ascompared to normal cells which is about −70 to −90 mv. These magneticfields can modulate the activity of sodium potassium pump that isresponsible for setting transmembrane potential. Recent studies inColumbia University have mapped the original frequency to control theactivity of numerous enzymes including the sodium potassium pump whichis described in the Journal of Biochemistry 53171-4/2001. The specificcellular machinery that turns the knob on and off in response to theelectromagnetic frequency has been recently identified as has beendescribed in the Journal of Cell Biochemistry GS Cell Biochem 81143-82001. Magnetic resonance therapy can combat cancer by directly inducingtumor cell death by activating the pro-apoptotic pathway, activation ofanti-tumor immune response and starving the tumor cells by inhibitingthe blood supply. Recent studies have demonstrated that specificfrequencies can inhibit cancer by blocking the tumor blood supply as hasbeen described by Anti Cancer Research 21388791 2001.

US Patent Publication No. 2007/0208249 discloses an apparatus for theapplication of what is claimed to be a rotational focused quantummagnetic resonance on any part of human body. The apparatus consist of aplurality of guns for the delivery of the quantum magnetic resonance, atravelling platform for carrying the person under treatment, anelectronic switching system for controlling the guns, said electronicswitching system being controlled by a main computer through an on boardmicroprocessor and means for cooling and dispersing the heat generatedduring the operation. Further in this system the 96 guns are used at anangle of 11.25°.

The following aspects of the US Patent Publication No. 2007/0208249 arenoted:

The construction of the guns as described in the patent specification isconstructed of special cores of high permeability material that isprecisely coiled with pure copper. It is apparent that such aconstruction is not the desired method capable of producing a focusedmagnetic field;

The placement of the guns at 11.25° cause interference due to themagnetic field generated by the two adjacent guns thereby causingmagnetic field in-homogeneity;

The system as disclosed cannot produce a “magnetic resonance” as thereis only a magnetic field and no associated radio frequencies to producethe magnetic resonance and therefore the concept of “for the delivery ofthe quantum magnetic resonance”, as stated in the patent specificationis misleading and consequently cannot be the basis for any treatment;the specification is devoid of any constructional details; thespecification does not disclose any method of treatment; thespecification also states that the magnetic field is rotating whichmeans that the field remains on all the time and the switching systemrotates the magnetic field a specific rate details of which are notdisclosed in patent specification; the above patent application neitherteaches the construction of the apparatus nor does it describe anymethod of treatment.

The conventional systems described above lack homogeneity of magneticfields which is an essential condition for effectiveness of treatments,and also flexibility of options in terms of field directions,orientations, etc. Further, most literature in this field lack thedesired details of the apparatus and/or the methods of treatment makingit practically impossible for a person trained in the art to eitherreproduce the reported effects and/or build the scantly describedapparatus.

There is a long felt need to provide a comprehensive system for inducingcellular regeneration and/or degeneration processes and methods oftreatment based on such processes that can be easily be applied todiverse states of tissue abnormalities or dysfunctions.

SUMMARY

In accordance with embodiments of the invention a SequentiallyProgrammed Magnetic Field (SPMF) therapeutic system and method comprisea plurality of arrays of magnetic field generators (MFGs) to producesequentially programmed pulsed magnetic fields at a focal region, thepulsing being controlled by a switching system operably linked to acomputer that generates the operating protocol based on an embeddedlogic that is dependent on the disease type and the treatment to beadministered.

The invention SPMF Therapeutic System is a system that induces cellularregeneration and/or the degeneration processes and methods of treatmentbased on such processes. Electromagnetic fields of certain frequencyranges and intensities are indigenous to living tissues and it has beenfound that inciting the inherent resonance by exogenous treatment usingan SPMF can induce cellular regeneration and/or degeneration processes.

Some embodiments of the invention provide an apparatus for generatingand applying a magnetic field to a desired tissue comprising: aplurality MFGs to produce sequentially programmed pulsed magnetic fieldsat a focal region; and a switching system to control the pulsingdependent on the disease type and the treatment to be administered.

Some embodiments of the invention further provide a tubular gantry forhousing the MFGs; wherein the MFGs are fixed circumferentially on thetubular gantry in regular intervals of about 15 to about 90 degrees withrespect to an adjacent MFGs with reference to the central axis of saidtubular gantry, which is the focal axis.

In some embodiments, the plurality of MFGs are operatively coupled inmated, opposed pairs, such that pairs of MFGs which are about 180degrees opposite to each other in the tubular gantry are energized atthe same time and out of phase so that the net magnetic flux passesthrough the core of the tissue or the centre of the region of interest.

In some embodiments, the invention provides an apparatus, furthercomprising a tubular gantry, defining from about 1 to about 12transverse planes with respect to the central axis of said gantry alongwhich the plurality of MFGs are located. In some embodiments, the gantrydefines from about 1 to about 9 transverse planes. In some embodiments,the gantry defines about 1 to about 5 transverse planes. On eachtransverse plane, about 2 to about 24 MFGs are disposed radially overthe circumference of the gantry. Diametrically opposite MFGs areoperatively coupled to form about 1 to about 12 pairs wherein each ofthe pairs can be excited to generate a magnetic field.

In some embodiments, circumferentially adjacent MFGs are displaced fromeach other by regular intervals of about 15 to about 180 degrees. Aswill be appreciated, the number of MFGs and the angle are directlyrelated to one another. A pair of MFGs will be about 180 degrees fromeach other. In an apparatus employing 24 circumferential MFGs each MFGwill be about 15 degrees from the next adjacent MFG. For example, whenthe MFGs are placed at regular intervals the following table sets forththe number of pairs, the number of MFGs in each transverse plane, andthe approximate angle between adjacent MFGs.

Pairs 1 2 3 4 5 6 7 8 9 10 11 12 MFGs 2 4 6 8 10 12 14 16 18 20 22 24Angle θ 180 90 60 45 36 30 25.71 22.50 20 18 16.4 15

In some embodiments of the invention, each MFG comprises a magneticallyconductive hollow cylindrical base body extending at one end into afunnel; a magnetically conductive rod-like structure extending throughsaid hollow cylindrical base into said funnel; and an electrical coilwound around the hollow cylindrical base body and the funnel.

In some embodiments the rod-like structure defines a frusto-conical endwhich extends into said funnel.

In some embodiments, an external magnetic shield is provided to the MFGfor limiting leakage of magnetism except through the funnel end.

In some embodiments, the cylindrical base body and funnel are made fromleaded steal, such as, but not limited to EN1A.

In some embodiments, the rod-like structure is a ferrite rod. Theferrite rod is about 35 mm long, and about 8 mm in diameter.

In some embodiments, the electrical coil is a copper wire. In someembodiments, the copper wire is 29G copper wire winding of about 46 mmand length of about 60 mm, and the number of turns is about 4200.

In some embodiments, the magnetic field generating device has animpedance of from about 80 and about 90 ohms

Some embodiments of the invention provide methods for inducing cellularregeneration and/or degeneration and for methods of treating certaindiseases, disorders, or conditions. Some embodiments provide a methodfor inducing cellular regeneration and/or degeneration in a patient inneed thereof comprising: applying a pulsed magnetic field to a desiredtissue in a sequential pattern. In some embodiments, the sequentialpattern is substantially rotary.

In some embodiments, the pulsed magnetic field is generated by aplurality of mated and opposed pairs of MFGs, wherein mated and opposedpair fire simultaneously and out of phase, and each pair is fired in asequential, substantially rotary pattern.

Some embodiments provide a method for treating cancer in a patient inneed thereof, comprising applying a pulsed magnetic field to a desiredtissue in a sequential pattern, wherein the pulsing frequencies are inthe range of about 120 to about 2000 Hz.

In some embodiments of the method of treating cancer comprises the stepof applying the pulsed magnetic field further comprises: applying asensitizing treatment phase at a frequency range of about 0.1 Hz toabout 600 HZ; and then applying a stimulating treatment phase afrequency range of approximately 600 Hz to about 2000 Hz. In someembodiments, the treatment may be administered for about 1 hour per dayfor about 28 days.

Some embodiments provide a method for treating arthritis in a patient inneed thereof, comprising applying a pulsed magnetic field to a desiredtissue in a sequential pattern, wherein the pulsing frequencies are inthe range of about 8 to about 50 Hz.

In some embodiments of the method of treating arthritis, the step ofapplying the pulsed magnetic field further comprises: applying asensitizing treatment phase at a frequency range of about 8 Hz to about20 HZ; and then applying a stimulating treatment phase a frequency rangeof approximately 12 Hz to about 40 Hz. The treatment is administered forabout 45 minutes to 1 hour per day for about 28 days.

In some embodiments, the invention provides a method for treatingneurodegenerative disorders in a patient in need thereof, comprisingapplying a pulsed magnetic field to a desired tissue in a sequentialpattern, wherein the pulsing frequencies are in the range of 30 Hz toabout 120 Hz.

In some embodiments, the step of applying the pulsed magnetic fieldfurther comprises: applying a sensitizing treatment phase at a frequencyrange of about 30 Hz to about 60 HZ; and then applying a stimulatingtreatment phase a frequency range of approximately 90 Hz to about 120Hz. The treatment may be administered for about 1 hour per day for about21 days.

In some embodiments, the neurodegenerative disorder to be treated isselected from Alzheimer's, Parkinson's, ALS, and Huntington's disease,in retinal degeneration, and other damage to sensory systems associatedwith stroke, head and spinal trauma, epilepsy, drug and alcohol abuse,infectious diseases, mental disorders, or from exposure to industrialand environmental toxicants, and chronic pain.

Additional features and advantages of the invention will be madeapparent from the following detailed description of illustrativeembodiments that proceeds with reference to the accompanying drawings.

BRIEF DESCRIPTION OF THE DRAWINGS

The foregoing and other aspects of the present invention are bestunderstood from the following detailed description when read inconnection with the accompanying drawings. For the purpose ofillustrating the invention, there is shown in the drawings embodimentsthat are presently preferred, it being understood, however, that theinvention is not limited to the specific instrumentalities disclosed.Included in the drawings are the following Figures:

FIGS. 1A and 1B are schematics of the section of magnetic fieldgenerating device;

FIG. 2 is a schematic of the ferrite rod;

FIG. 3 shows a block diagram of the embedded system;

FIG. 4 is a schematic of system configuration;

FIG. 5 shows an exemplary wound magnetic field generating device;

FIG. 6 shows an exemplary wound magnetic field generating device;

FIG. 7 shows a layout of exemplary MFG devices;

FIG. 8 shows a layout of exemplary MFG devices;

FIGS. 9A-9E diagnostic images of a 30 year old female—Synovial Sarcomawith Mets in right lung and Mediastinal Lymph Nodes; (9A diagnostic CTScan, 9B pretreatment CT Scan, 9C Mid-treatment CT scan, 9D immediatelypost-treatment scan, 9E—post treatment scan);

FIGS. 10A-10L are diagnostic images of a 55 year old male—Left PosteriorFrontal—GBM (WHO Grade—IV); (10A, B, C pretreatment scans, 10D, E, Fimmediately post-treatment scans, 10G, H, I 4 months post treatment,10J, K, L, 9 months post treatment);

FIGS. 11A-11D is an exemplary case summary for Osteo Arthritis;

FIG. 12 is a pictorial representation of a human cell and organelles;

FIG. 13 illustrates an outline of the ATP-synthase macromolecule showingits subunits and nano machine traits;

FIG. 14 shows Centriole in the normal cell cycle;

FIG. 15 shows Centriole in the abnormal cell cycle;

FIG. 16A is a flow chart for patient treatment of cancer;

FIG. 16B is a flow chart of a proposed mechanism of action in accordancewith an embodiment of the invention;

FIG. 17A is a flow chart for patient treatment of arthritis;

FIG. 17B is a flow chart of a proposed mechanism of action in accordancewith an embodiment of the invention;

FIG. 18 is a flow chart for patient treatment of neuro-tinnitus; and

FIG. 19 is a flowchart illustrating exemplary logic for a sequentiallyprogrammed magnetic field (SPMF) therapeutic system.

DETAILED DESCRIPTION OF ILLUSTRATIVE EMBODIMENTS

The Sequentially Programmed Magnetic Field (SPMF) therapeutic system isa computer controlled device which generates sequential pulsed magneticfields, by employing a plurality of Magnetic Field Generators (MFGs).The magnetic field can be precisely controlled and applied onto thecells and/or tissues that require the treatment. The MFGs are fired in aprogrammed sequence to facilitate the focusing of the magnetic field andis believed to result in better patient outcomes.

Inciting the inherent resonance by exogenous treatment using SPMFs caninduce cellular regeneration and/or degeneration processes. In the caseof regeneration and degeneration of cells, the pulsing frequencies arein the range of about 0.1 to about 2000 Hz based on the indication ofthe disease type which is determined by the patient's MRI, CT,Ultrasound or other diagnostic information.

As such, the apparatus may be used to treat conditions where cellulardegeneration and/or regeneration is advantageous. In some embodiments,the apparatus may be used in: (i) a method for treating arthritis bycausing regeneration of cartilage with the help of the aforesaidapparatus; (ii) a method for degeneration of cancerous tissues bysubjecting them to magnetic field generated and applied by the aforesaidapparatus, (iii) a method for treating diabetes by regenerating theislet cells by the use of the aforesaid apparatus; (iv) a method totreat spinocerebellar degeneration and/or multiple sclerosis by the useof the aforesaid apparatus; (v) a method to treat neuro degenerativedisorders, such as, but not limited to, Alzheimer's, Parkinson's, ALS,and Huntington's disease, in retinal degeneration, and other damage tosensory systems (e.g., visual, auditory, somatosensory), in stroke, headand spinal trauma, epilepsy, in drug and alcohol abuse, in infectiousdiseases, in exposure to industrial and environmental toxicants, and,perhaps, in mental disorders and chronic pain; (vi) a method fortreating non-healing fractures and other bone conditions; (vii) a methodfor treating various other conditions that could benefit fromregeneration or degeneration of tissues.

An apparatus for inducing a SPMF in biological tissue(s) comprises meansfor generating and applying magnetic fields to the biological tissue(s)from one or more pairs of oppositely placed means for generating andapplying magnetic fields. The magnetic field is generated simultaneouslyby mated opposed pairs of MFGs. In some embodiments, the magnetic fieldis applied in a sequential programmed manner by different mated opposedpairs. In some embodiments, a magnetic field of the same strength isgenerated and applied to the said tissue(s) from each oppositely placedMFG in each pair. The sequential application may be conducted in matedopposed pairs or in selected groups of mated opposed pairs of MFGs. Thesequential program, in some embodiments, is generally rotary in nature,wherein the firing sequence of the MFGs generally flowscircumferentially from one adjacent MFG to the next. In the case of thesystem having multiple rows of MFGs, in some embodiments, the firingsequence continues to the next adjacent row for sequentialcircumferential firing of the MFGs, and so on until the desired programis completed.

Referring to FIGS. 1A and 1B, each MFG comprises a hollow cylindricalbase body ending in a funnel, made of material capable of magneticconduction. The body houses a rod-like structure having good magneticconductivity. An electrical coil is wound around the hollow base bodyand its funnel end and connected to an electrical supply to generatemagnetic field. An external cover may be optionally provided to minimizeor prevent leakage of magnetic field. The one or more pairs of MFGs arehoused in a tubular gantry, preferably in transverse rows of more thanone and circumferentially at an angle of about 15 to about 90 degreeswith respect to one another based on the focal point located on atransverse axis of the tubular gantry, where the biological tissue to betreated is placed.

The methods proposed by this invention for regeneration or degenerationof tissues in the treatment of the aforesaid ailments, and others,involves planning the exposure of the tissues to a SPMF generated by theapparatus and thereby to induce a pulsed magnetic field. The extent ofthe exposure to such pulsed magnetic field would depend upon the amountof progression of the condition, for example the amount of degenerationthat is already set in and other factors depending on the condition tobe treated. The plan results in a determination of one or more of thefollowing, frequency to be used, field width, field intensity, durationof each pulse, pattern of the sequential program, duration of individualtreatments, number of treatments required, etc.

Upon application, the area to be treated is aligned at the focal point.A sensitizing treatment phase may be used depending upon the treatmentplan and the condition to be treated. Then, a stimulating treatmentphase wherein the magnetic field is generated and applied according tothe plan. The magnetic field is generated and applied in a sequentialpattern. After the desired number of treatments, the patient can bereevaluated and the plan adjusted and/or reassessed if necessary.

In the case of regeneration and degeneration of cells, the pulsingfrequencies are in the range of about 0.1 Hz to about 2000 Hz based onthe indication of the disease type which may be determined, for example,by either the patient's MRI, CT, Ultrasound or other technique. In someembodiments, the pulsing frequencies are in the range of about 120 Hz toabout 2000 Hz. In some embodiments, the pulsing frequencies are about 5Hz to about 120 Hz. In some embodiments, the pulsing frequencies are inthe range of about 1 Hz to about 600 Hz. In some embodiments, thepulsing frequencies are about 8 Hz to about 50 Hz. In some embodiments,the pulsing frequencies are about 30 Hz to about 120 Hz.

The Apparatus

In accordance with embodiments of the invention a SequentiallyProgrammed Magnetic Field (SPMF) therapeutic system and method comprisea plurality of arrays of MFGs to produce sequentially programmed pulsedmagnetic fields at a focal region, the pulsing being controlled by aswitching system operably linked to a computer that generates theoperating protocol based on an embedded logic that is dependent on thedisease type and the treatment to be administered.

Generally, the apparatus comprises a plurality of MFGs 100 to generateand apply magnetic field. The MFGs 100 are fixed circumferentially on atubular gantry 101 in regular intervals of about 15 to about 90 degreeswith respect to adjacent MFGs 100 with reference to the focal axis 500.

Each MFG 100 consists of a hollow cylindrical base body 2 extending intoa funnel 4. It is made of material capable of magnetic conduction; a rodlike structure (FIG. 2, 30) having good magnetic conductivity fixedwithin the cylindrical base body 2 extending into the funnel 4; anelectrical coil 95 wound around the hollow cylindrical base body 2 andthe funnel 4. (Electrical coil 95 is not shown in FIG. 1A for clarity.

The electrical coil 95 is connected to an electrical supply. Theelectrical coil 95, on passing of electric current generates magneticfield. The funnel end 4 of each MFG 100 faces inside the tubular gantry101 toward the focal axis 500.

The rod like structure in the MFG increases the strength and uniformityof the magnetic field thereby increasing the efficacy of the apparatus.

The MFGs are located at such an angle θ and at such a distance D fromeach other so as to reduce or eliminate interference between themagnetic field generated by the given means and the residual magneticfield of the adjoining means. FIG. 3 shows a block diagram of theembedded system, θ shows the angle between adjacent MFGs. The distancebetween circumferentially adjacent MFGs is shown as D, and depends onthe size of the machine, the number of MFGs, and the angle θ betweenthem. In one exemplary arrangement with 24 circumferential MFGs, θ is 15degrees and the distance D between adjacent circumferential MFGs is129.25 mm

Shielding of housing of the MFGs and/or the system by an external covermay be employed to limit or prevent leakage of the magnetic fieldthereby increasing the efficacy of the apparatus and making it safe tooperate.

The apparatus may contain additional components that make the apparatusmore useable or user friendly or enhance performance. For example: a fancan be employed to circulate air around the tubular gantry 101 toprevent collection of dust and static charge which potentiallyinterferes with the magnetic field. An external cover may be provided toshield the tubular gantry 101 against leakage of magnetic field. A bedon a supporting stand having cushion may be used, sliding a patientlying thereon into the tubular gantry 101 with the help of supportingmotor (not shown), gear railings, bearings and supporting railings. Assuch tissues of the patient which are to be treated can be positioned atthe focal point where the magnetic field generated from the MFGs 100 isfocused.

In most other treatment devices with energizing coils, the coils areunidirectional. In this method, the coils are bidirectional because thecoils which are approximately 180 degrees opposite to each other in thetubular gantry 101 are energized at the same time and out of phase sothat the net magnetic flux passes through the core of the tissue or thecentre of the region of interest. That is, mated opposed pairs of MFGsfire simultaneously from opposite directions. The constant switching orthe energizing of coils in a rotary pattern causes the focusing to occurin a relatively small area which is the tissue to be treated. This highspeed switching causes focusing similar to that achieved in theprinciples of tomography or computerized tomography. The net magneticflux can be directed at the center of the region of interest (i.e. focalpoint) with very little emission required from each of the MFGs.

Data is fed into a computer coupled to and controlling the apparatus.Based on the disease type, the duration, and nature of the disease etc.,the computer software calculates the duration of the exposure, the pulsefrequency, the frequency of the firing and the amount of SPMF dependingon the patient and the disease.

The following embodiments describe how the entire system functions as acomprehensive apparatus to produce the SPMF specifically for aparticular disease type. The embedded system comprises a computer, highspeed processing controller, power supplies, MFGs, a cylindrical gantrythat, in some embodiments, includes a total of 216 MFG's that producethe sensitizing and stimulating frequency's required to treat specificdisease types. More or fewer MFG's could be employed depending upon theapplication, size and arrangement of the apparatus. Particularly, itshould be noted that full body apparatus are contemplated as shown inthe drawings, but smaller models suitable for treatment of, e.g. theelbow or knee are also contemplated.

In accordance with one embodiment of this invention, the sequentialprogrammed magnetic field generation system may include:

an embedded system comprising a high speed processing microcontrollerconfigured with a power drive module that comprises a digital to analogconverter for set voltage reference of regulated field strength, pulsewidth modulation circuit, optional current sensing circuit configuredwith operational amplifier, digital to analog converters, PWM supportedASICS & MOSFETs, optical isolations to ensure complete isolation betweenprocessor system and analog system;

a pulse drive module comprising power MOSFETs in “H” bridge formationwith heat sinks, gate drive systems through optically isolated drivemodules and a set of transistors, optical isolation system for isolatingmain processor module with power MOSFETs system, a set of LED's forphysical verification of proper excitation of magnetic coils, powerrectifier's fuses and surge protection system;

a step down transformer configured with main AC power supply; personalcomputer; set of fault monitoring LEDs;

wherein the embedded system is provided with interrupt provision thatenables serial communication, timers for controlling the sequentialoperation of exciting the coils of the core, power monitoring facilitywherein if voltage drops below designed value, the critical parametersare saved in the flash memory of central processing unit;

wherein the embedded system is configured with a plurality of MFGs;

wherein plurality of such MFGs are circumferentially disposed on theinternal diameter of a cylindrical structure such that the devices aredisposed diametrically opposite to each other in each cross section ofthe cylinder;

wherein the surface of the cylindrical structure is mounted with suchMFGs in longitudinal direction;

wherein the magnetic field generating device is controlled by theembedded system to generate tailored pulsed magnetic fields directed toa region of interest or focal point;

an initialization module wherein peripherals and sub systems areconfigured wherein baud rate for serial transfer of data between PC andprocessor, timer periodicity and wait time for packet transferset/initialized;

a serial—data receiving module to receive the data and command from thepersonal computer and validate the packets received, accept/rejectpackets and send acknowledgment;

a packet evaluation module to evaluate the packet for correct nodeaddress, CRC check and ensure commands and data are within theacceptable limits;

an acknowledgement module to transmit any and requested data packets tothe personal computer;

an executive command module to initiate process in respect of treatmentsequence, stop on set time expiry, pause or stop command issued bysystem operator from the personal computer;

wherein the diametrically disposed coils of the paired MFGs areconnected in series and subjected at a time to a rectangular pulseoperating out of phase with respect to each other to produce aneffective magnetic field at the region of interest; wherein the pulsecharacteristics are selected from frequency of about 0.1 Hz to about 2KHz, pulse count of about 2 to about 50, current of about 0.1 to about 5amps, voltage from about 20 to about 65 V, producing effective magneticfield of about 0.01 to about 5 mT, wherein the time duration between theswitching off and the switching on of the adjacent pair diametricallydisposed MFGs is about 1 msec to about 5 msec.

These features of the processes have been illustrated in FIG. 19—systemflowchart.

FIG. 1A and FIG. 1B describe one embodiment of a magnetic fieldgenerating device (MFG) 100 employed in the magnetic field generatingsystem. As shown, the magnetic field generating device 100 may comprisea disc shaped base mounting member 1 wherein cylindrical base body 2 isdisposed substantially perpendicular to the first surface 6 of the discshaped mounting member 1 and stands upwards from the first surface ofthe disc shaped mounting member. A mounting provision 90 as indicated inFIG. 6 (as seen in the bottom view of the mounting member 1) in the formof a preferably threaded hole is provided in the center of thecylindrical base body 2 wherein the opening of the hole is on the secondsurface 9 of the disc shaped mounting member 1. The other end portion 3of the cylindrical base body 2 develops up in to a conical structure orfunnel 4 as seen in FIG. 1A with outwardly diverging slant lateralsurface (of generation) that forms the surface of the cone wherein thecross section of the apex portion which is the apical portion of thefunnel 4 is equal to the diameter of the cylindrical base body 2. A baseportion is provided with a rim like substantially flat portion 10.

A concentric cavity 11 is provided inside the cylindrical base body 2wherein the cavity opens in the inner portion 15 of the conical member 4at the opening 7 that elevates inside the conical portion wherein theopening 7 forms apical portion of a second conical frustum 20 comprisinglateral surface of generation 8 extending downwards towards thecylindrical base body 2 wherein the lateral surface 8 intersects theinside lateral surface of the conical member 4 to form annular space 16as shown in FIG. 1B which is the top view of the FIG. 1A. The cavity 11is adapted to receive a ferrite rod 30 (FIG. 2) wherein one of the endportions 31 is in the form of a truncated conical geometry.

The outer surface 21 of the cylindrical base body 2 is provided with oneor plurality of axial slots 25 wherein portion of the slot extends inthe lateral surface of generation of the conical member 4. The mountingmember 1 is provided with one or plurality of holes 26 as illustrated inFIG. 5 and FIG. 6 for insertion of wire/conductor terminals 91 and 92.

The outer surface of the conical member 4 and the cylindrical base body2 may be wrapped with a magnetically permeable paper (e.g., elephantpaper). An electrical coil 95 is wound over the entire outer surface toform the magnetic field generating device which is illustrated in FIG.5. The electrical coil 95 may be a copper conductor. It can be seen thatthe electrical coil 95 is wound from the mounting member 1 up to the rimlike portion 10. The conductor terminals 91 and 92 are inserted from theholes 26 provided in the base 1 as shown in the FIG. 5 and FIG. 6(bottom view).

In some embodiments, the cylindrical base body 2 is made from EN1Aleaded steel, the ferrite rod is about 35 mm in length, about 8 mm indiameter and about 25 degree slope, and the diameter of the exemplary29G copper wire winding is about 46 mm and the length of about 60 mm Thenumber of turns is about 4200. This arrangement results in an impedanceof between about 80 and about 90 ohms

FIG. 3 and FIG. 7 depict circumferential disposition of the plurality ofMFGs 100 on a cylindrical structure 101 subtending at an angle of about15 degrees to about 90 degrees to each other based on the applicationand end use. The MFGs 100 are arranged in pairs disposed diametricallyopposite to each other about focal axis 500. FIG. 4 depicts front andside views of the structure wherein the surface of the cylindricalstructure 101 includes multiple MFG pairs mounted in rows wherein eachof the rows comprises a plurality of the MFGs as shown in the frontview.

In some embodiments, the MFGs are arranged in a clustered configurationon the tubular gantry 101 as depicted in FIG. 7. In some embodiments,the gantry 101 may be divided into a plurality of segments. For example,it may be divided into three segments A, B and C as indicated in theFIG. 7. It may be noted that the segments in the FIG. 7 are indicatedseparately for better elaboration and appreciation of the aspect ofclustered configuration only, it should not be construed that the threesegments of the cylindrical structure are physically separated. Each ofthe segments is provided with rows arranged in the longitudinaldirection along the focal axis 500 disposed over the circumference ofthe segment wherein each of the segment rows 200 include three MFGs 100a, 100 b and 100 c. The devices in other rows are indicated with dashedlines in the FIG. 7. In the embodiment depicted in FIG. 7, there aretotal 9 MFGs in one longitudinal row across the gantry clustered into aset of three devices on each of the segments A, B and C.

In the illustrated embodiment, there are 24 MFGs disposed radially overthe circumference of the gantry 101 in each transverse plane to the axis500. The diametrically opposite devices are paired to form twelve suchpairs wherein each of the pairs is excited to generate a magnetic field.Assuming three such transverse planes in each segment corresponding toeach of the MFGs (such as 100 a, 100 b and 100 c), there are 24 devicesin each transverse plane and three such planes totaling 72 MFGs in eachsegment. In another embodiment, the number of such devices in each rowand transverse plane may vary depending on end application.

The MFGs of each of the segments are configured or operatively coupledto a control means. In some embodiments, there are three such controlmeans corresponding to the three segments. The control means isconfigured with the embedded system for controlling magnetic fieldstrength, sequence and frequency of field excitation in a tailoredmanner according to the treatment protocol.

The MFGs 100 of the system are configured with the embedded system 50that is represented in the form of a block diagram in FIG. 3. Theembedded system 50 comprises a high speed processor 51 wherein in oneembodiment the processor is an analog device 32 bit ARM based processorworking at about 40 MHz frequency microcontroller comprising peripheralssuch as serial communication interface, circuit for set voltagecontroller reference system and Logic IC'S for coordinated operation forpower MOSFETs at digital TTL level that is configured with, for example:

a power drive module comprising digital to analog converter for setvoltage reference of regulated field strength, pulse width modulationcircuit, optional current sensing circuit configured with operationalamplifier, digital to analog converters, PWM supported ASICS & MOSFETs.Further, the module has optical isolations 54 to ensure completeisolation between processor system and analog system;

pulse drive module comprising power MOSFETs in “H” bridge formation withheat sinks, gate drive systems through optically isolated drive modules& set of transistors, optical isolation system for isolating mainprocessor module with power MOSFETs system, set of LED's for physicalverification of proper excitation of magnetic coils, power rectifier'sfuses & surge protection system;

step down transformer 59 configured with main AC power supply 60;

personal computer 58;

set of fault monitoring LEDs;

wherein the embedded system is provided with interrupt provision thatenables serial communication, timers for controlling the sequentialoperation of exciting the magnetic coils of the core, power monitoringfacility wherein if voltage drops below about 3.3 volts, the criticalparameters are saved in the flash memory of central processing unit;

wherein the main AC power supply of about 230V, about 50 Hz is steppeddown to the desired voltage level using the step down transformer 59.Further the stepped down voltage is rectified, filtered and regulated inthe power supply circuitry 61 that comprises first circuitry for DCVoltages of about +15V and about −15V that is necessary for operationalamplifier, second circuitry for DC Voltage of about 5V that is necessaryfor logical circuitry, third circuitry for DC Voltage of about 5V andpower on indicator circuitry that uses LED as visual indicator. The highspeed processor 51, optical isolation circuitry 54 comprising LED andphototransistor integrated together wherein the circuitry 54 providesisolation between analog and digital circuit. The voltage signal from 54is fed to the field control bridge circuitry 52 along with the signalfrom the processor 51 that transmits signal based on pulse strength,pulse frequency, pulse Sequence & pulse counts based on the object to betreated. The signals from 54 and 52 are fed to the bridge circuitry 52that comprises power MOSFETs. The pulse duration, pulse frequency andsequence is controlled using input from the processor.

As shown in FIG. 19, the embedded system operation module may comprise:

initialization module wherein peripherals and sub systems are configuredwherein baud rate for serial transfer of data between PC and processor,timer periodicity and wait time for packet transfer is set/initialized;

serial—data receiving module to receive the data & command from thepersonal computer and validate the packets received, accept/rejectpackets and send acknowledgment; packet evaluation module to evaluatethe packet for correct node address, CRC check and ensure commands anddata are within the acceptable limits;

acknowledgement module to transmit any and requested data packets to thepersonal computer;

executive command module to initiate process in respect of treatmentsequence, stop on set time expiry, pause or stop command issued bysystem operator from the personal computer;

In one embodiment, the embedded system software may be structured to:

Call sub-routines to perform the specific tasks;

System Initiation which starts the peripheral and sub systems as derivedby the software;

Validate all data that is being transmitted or received;

Start, executive, command and monitor specific protocol sequences;

Initiate the start sequence, the stop sequence, the frequency and powerrequired for the specific protocol;

Set the pulse strength, pulse frequency, pulse count and pulse counts;

Save all critical parameters in the flash memory of the processor in theevent of a power failure.

Methods

In the case of regeneration and degeneration of cells, the pulsingfrequencies are in the range of about 0.1 to about 2000 Hz based on theindication of the disease type which was determined, for example, byeither the patient's MRI, CT Ultrasound, or other diagnosticinformation.

Exposure of cancer cells to SPMF therapy normalizes the cell membranepotential, thereby halting the process of cell proliferation, followedby programmed cell death (Apoptosis). A cascade of effects followsnormalization of cell membrane potential, i.e. increased influx ofCalcium, Potassium ions and Oxygen and efflux of Na and H₂O out ofcells, and reduction in intracellular acidity.

The normal cells are substantially unaffected by the SPMF. Furthermore,the signals are modulated depending on the proton density of the tumortissue and impedance of normal cells mitochondrial sensors. The energydelivered during the therapy is well within the safety norms prescribedby the International Commission for Non-Ionizing Radiation Protection(ICNIRP).

In one of the embodiments, the SPMF is used in the treatment of cancerby causing degeneration of tumor cells wherein the pulsing frequenciesare in the range of about 120 to about 2000 Hz.

For cancer, the specific relationships and algorithms used areestablished for the signal intensities between the skin and the tumorhence would cause differential attenuation of these SPMF. First theregion of interest and the center of the tumor are marked by a softwareprogram, the pixel intensities are calculated along the skin to thecenter of the tumor about every 15 degrees (or other increment) whichcorresponds to the placement of each MFG. This information is input intothe computer so that the energizing of each MFG can be different basedon the field required for a particular MFG. Signal strength is derivedfrom the MRI, CT Ultrasound image or other diagnostic information. Oncethis is calculated, the dose information is input into the computer. Insome embodiments, the treatment protocol first sensitizes the cellularstructure and then stimulates the cell to start the regeneration processand initiate the degeneration process. In some embodiments, thetreatment protocol first sensitizes the cellular structure at afrequency range of about 0.1 Hz to about 600 HZ and then stimulates thecellular structure at a frequency range of approximately 600 Hz to about2000 Hz to start the regeneration process and initiate the degenerationprocess. In some embodiments, the treatment would be for a duration ofabout 1 hour per day for about 28 days.

The methods of using SPMF therapy for regeneration involves planning ofthe exposure which is based on the amount of degeneration that isalready set in and other factors relevant to the particular condition tobe treated. Once the dose planning is done, the patient is marked usingultrasound or other techniques. At the same time, the joint is evaluatedfor any effusion and marking is done at one or two points where thetherapy needs to be delivered. Once the patient is marked, the patientis taken into the SPMF system, for example on a sliding platform, andthe magnetic field is focused on to the region of interest, for examplewith the help of the laser guide, and the treatment runs for the periodof time that is designated based on the factors mentioned above.

In one of the embodiments, the SPMF is used in the treatment ofarthritis by causing regeneration of cartilage wherein the pulsingfrequencies are in the range of about 8 to about 50 Hz.

For Arthritis a predetermined dose profile is formed based on the gradeand severity of the arthritis and the permittivity index. Patients whohave early stage arthritis receive a low sensitizing frequency in therange of about 8 Hz to about 20 Hz, a stimulating frequency in the rangeof about 12 Hz to about 40 Hz. Patients who have severe arthritis and ahigh permittivity index receive a sensitizing frequency of about 10 Hz,and a stimulating frequency up to about 40 Hz. In some embodiments, thetreatment is for a duration of about 45 min to about 1 hour per day forabout 21 days.

The results confirm significant regeneration of cartilage, increase inthe strength and stability of, e.g., the knee joint and improvement inquality of life, as measured with a MRI system and internationallyaccepted American Knee Society rating system.

In neuro degeneration, the progressive loss of nerve cells occurs inaging and in neuro degenerative disorders, such as Alzheimer's,Parkinson's, ALS, and Huntington's disease, in retinal degeneration, andother damage to sensory systems (e.g., visual, auditory, somatosensory),in stroke, head and spinal trauma, epilepsy, in drug and alcohol abuse,in infectious diseases, in exposure to industrial and environmentaltoxicants, and, perhaps, in mental disorders and chronic pain. Thetreatment pulsing frequencies for the neuro protocols are in the rangeof about 30 Hz to about 120 Hz. The treatment protocol first sensitizesthe cellular structure at a frequency range of about 30 Hz to 60 HZ andthen stimulates the cellular structure at a frequency range of about 90Hz to about 120 Hz to start the regeneration process. The treatment timeis approximately 1 hour a day for 21 days.

For Ménière's disease the pulsing frequencies are in the range of about8 to about 30 Hz.

In yet another embodiment of the invention, the SPMF is used to treatnon-healing fractures or in treatment of diabetics wherein therequirement is to regenerate the islet cells.

In some embodiments, the SPMF is used for a variety of degenerative orregenerative applications where specific parameters can be determinedthrough similar techniques as used and described above.

Methods of Treatments Using SPMF

SPMF has been used to treat the following disease types; cancer,arthritis, neuro degenerative diseases. The follow sections describe themethods of treatments including non limiting examples to illustrate theutility of the SPMF system.

Treatment Protocols for Cancer—An exemplary patient process flow chartfor cancer is illustrated in FIG. 16.

In cancer the process of treatment starts with first localizing thetumor which would be the region of interest (ROI) using the ideal formof imaging i.e. MRI, CT or ultrasound. For example, head and neck tumorsare best seen on MRI and lung tumors are best seen on CT scan andthyroid tumors are best viewed on an ultrasound. Once the tumor islocalized a specific proton density image (short TE and a long TR) isdone through the center of the lesion. Using this proton density image,specific algorithms are obtained based on signal intensities between theskin and the tumor which are different with different tissues and itwould cause differential impudence of the SPMF. For the proton densityimage, the ROI that would be a tumor is marked and uploaded on to ageneric software by which these densities are converted to pixelintensities from the skin to the center of the tumor. The intensitiesare calculated along lines drawn at about 15 degrees from the center ofthe tumor which would denote the placement of each MFG. The parametersof the signal strength would be different based on how much penetrationand frequency is required from the MFG coil based on the intensities oftissue that are between the skin and tumor. The treatment protocol lastsfor a period divided into 2 or more phases of predetermined durationwhere in the first duration the frequencies applied are the frequencieswhich essentially sensitize the cell membrane and are followed bysubsequent duration(s) of stimulating frequency which finally causeschange in cell membrane potential. In one embodiment, the treatmentprotocol lasts for approximately 1 hour and is divided into 2 phaseswhere the first 30 minutes (approximately), the frequencies applied arethe frequencies which essentially sensitizes cell membrane and isfollowed by 30 minutes (approximately) of stimulating frequency whichfinally causes change in cell membrane potential. Different protocolsare set based on proton densities of the tumor. Tumors having highproton density are treated with a high ratio and sensitizing andstimulating that could go to the range of around 2000 Hz. Tumors withlow density are treated with lower sensitizing and stimulatingfrequencies ratio and these frequencies range to about 120 Hz.

Algorithm for High Proton Density

1) Minimum Density=3^(rd) minimum of Pixel Value

-   -   a. The minimum density is derived by discarding the 2 lowest        recorded proton density pixel values (formula b) and the program        will register the 3^(rd) lowest value as the “minimum density”.        This methodology is being used because the density value of air        is very low and would distort the calculation.    -   b. S=PD exp(−TE/T2)(1−exp(−TR/T1))(n)        -   i. In this equation, S is the brightness (signal) measured            at some particular point in the image—at some particular            “pixel”; PD is “Proton Density”, the number of hydrogen            atoms in the region corresponding to that pixel; and T1 and            T2 are the corresponding time constants for that pixel.

2) Maximum Density=3^(rd) Maximum of Pixel Value

-   -   a. The maximum density is derived by discarding the 2 highest        recorded proton density pixel values (formula b) and the program        will register the 3^(rd) highest value as the “maximum density”.        This methodology is being used because the density value of bone        is very high and would distort the calculation.    -   b. S=PD exp(−TE/T2)(1−exp(−TR/T1))(n)        -   i. In this equation, S is the brightness (signal) measured            at some particular point in the image—at some particular            “pixel”; PD is “Proton Density”, the number of hydrogen            atoms in the region corresponding to that pixel; and T1 and            T2 are the corresponding time constants for that pixel.

3) Average Density=(Sum of Pixel Values/No. Of Pixel Values)

-   -   a. The average density is derived by dividing the sum of the all        the Pixel Values in the region of interest by the total number        of pixels in the region of interest

4) Skin To Target=Root((xe−xs)̂2+(ye−ys)̂2)

-   -   a. The Skin to Target value is derived by the root value of xe        (x axis target)−xs (x axis Skin) squared plus ye (y axis        target)−ys(y axis skin) squared

5) Sensitizing Frequency=Min density*6.28

-   -   a. The minimum density as described in (1a) is multiplied by        6.28 which is 2π

6) Download Sensitizing Frequency=HEX(65536−(500000/SeF))

-   -   a. This equation is the hexadecimal input for the Sensitizing        Frequency

7) Stimulating Freq=Max density*1.57

a. The maximum density as described in (2a) is multiplied by 1.57 whichis π/2

8) Download Stimulating Frequency=HEX(65536−(500000/StF))

-   -   a. This equation is the hexadecimal input for the Stimulating        Frequency

9) k=(Maximum Density*Minimum Density)/(“AvgDensity”)

-   -   a. k is used to calculate the pulse count and is derived from        multiplying the maximum density by the minimum density and        divided by the average density

10) Pulse Count Sensitizing=Sensitizing freq/k

-   -   a. The pulse count for sensitizing is derived by dividing the        sensitizing freq by k

11) Pulse Count Stimulating=Stimulating freq/k

-   -   a. The pulse count for stimulating is derived by dividing the        stimulating freq by k

Algorithm for Low Proton Density

1) Minimum Density=3^(rd) minimum of Pixel Value

-   -   a. The minimum density is derived by discarding the 2 lowest        recorded proton density pixel values (formula b) and the program        will register the 3^(rd) lowest value as the “minimum density”.        This methodology is being used because the density value of air        is very low and would distort the calculation.    -   b. S=PD exp(−TE/T2)(1−exp(−TR/T1))(n)        -   i. In this equation, S is the brightness (signal) measured            at some particular point in the image—at some particular            “pixel”; PD is “Proton Density”, the number of hydrogen            atoms in the region corresponding to that pixel; and T1 and            T2 are the corresponding time constants for that pixel.

2) Maximum Density=3^(rd) Maximum of Pixel Value

-   -   a. The maximum density is derived by discarding the 2 highest        recorded proton density pixel values (formula b) and the program        will register the 3^(rd) highest value as the “maximum density”.        This methodology is being used because the density value of bone        is very high and would distort the calculation.    -   b. S=PD exp(−TE/T2)(1−exp(−TR/T1))(n)        -   i. In this equation, S is the brightness (signal) measured            at some particular point in the image—at some particular            “pixel”; PD is “Proton Density”, the number of hydrogen            atoms in the region corresponding to that pixel; and T1 and            T2 are the corresponding time constants for that pixel.

3) Average Density=(Sum of Pixel Values/No. Of Pixel Values)

-   -   a. The average density is derived by dividing the sum of the all        the Pixel Values in the region of interest by the total number        of pixels in the region of interest.

4) Skin To Target=Root((xe−xs)̂2+(ye−ys)̂2)

-   -   a. The Skin to Target value is derived by the root value of xe        (x axis target)−xs (x axis Skin) squared plus ye (y axis        target)−ys(y axis skin) squared

5) Sensitizing Freq=Average density*3.14

-   -   a. The average density as described in (3a) is multiplied by        3.14 which is π

6) Download Sensitizing Frequency(65536−(500000/SeF))

-   -   a. This equation is the hexadecimal input for the Sensitizing        Frequency

7) Stimulating Freq=Max density*3.14

a. The maximum density freq as described in (2a) is multiplied by 3.14which is π

8) Download Stimulating Frequency=HEX(65536−(500000/StF))

a. This equation is the hexadecimal input for the Stimulating Frequency

9) k=(Maximum Density*Minimum Density)/(“AvgDensity*3.14* 3.14”)

-   -   a. k is used to calculate the pulse count and is derived from        multiplying the maximum density by the minimum density and        divided by the average density which is multiplied by π*π

10) Pulse Count Stimulating=Stimulating freq/k

-   -   a. The pulse count for stimulating is derived by dividing the        stimulating freq by k

If PCSt>=50 Then

PCSt=50

Else If PCSt<=10 Then

PCSt=10

11) Pulse Count Sensitizing=(sensitizing freq/stimulating/freq)*PCSt

The pulse count for sensitizing is derived by dividing the sensitizingfrequency by the stimulating frequency and multiplied by pulse countsimulating.

Effect of SPMF Therapy in Tissue Degeneration Processes:

Even though there have been many advances in molecular biology andgenetics, no uniform genetic or DNA damage pattern has been demonstratedin all types of cancers. Despite heterogeneity of cancer there arecertain common features in all types of cancers, for example canceroustissue is morphologically and functionally more primitive than itstissue of origin, has uncontrolled growth, has capacity to invadesurrounding tissue, metastasize at different sites and derive its energyby glycolysis and the cells have low membrane potential (e.g., −15 mV to−30 mV).

Furthermore, the observation that fusion of normal cytoplasm withmalignant cell nucleus yields 0% tumor while fusion of normal cells withmalignant cell cytoplasm, produce cells with 97% of malignancy. Thispoints to the fact that DNA damage is not the cause, but the result ofunregulated, excessive proliferation of cells and loss ofself-correcting mechanism. The cause of carcinogenesis lies in themicro-environment of nucleus, which is cell membrane, electron-protonhomeostasis and reversion to glycolytic state.

Role of Transmembrane Potential in Carcinogenesis:

All living cells have membrane potential of about −70 mv. In healthytissue inside of cell is negative relative to exterior, but when tissuesare injured sodium & water flow into cells with loss of potassium,magnesium & zinc, lowering the cell membrane potential.

Healthy cell membrane potential is strongly linked to membrane transportmechanism as well as DNA activity and protein synthesis. Therefore theinjured cells which cannot maintain normal cell membrane potential willhave electronic dysfunction that will impede repair and regenerationprocess.

It is a well known fact that the cell membrane potential of cancer cellsis about −15 mV to about −30 mV. Exposure of cancer cells to SPMFnormalizes this potential, thereby arresting the process of cellproliferation. A cascade of effects follows normalization of cellmembrane potential, i.e. increased influx of Calcium, Potassium ions andOxygen and efflux of Na and H₂O out of cells, and reduction inintracellular acidity. SPMF also increases the impedance ofmitochondrial membrane potential and restores energy production.

In 1971, Cone postulated a functional relationship between transmembranepotential (TMP) and mitotic activity in general, including both normal,proliferative activity (eg, growth, healing wounds) and malignancy.Specifically he proposed that cells with normal TMP demonstrated virtualabsence of mitotic activity while cells with low TMP showed greatlyincreased proliferation. He demonstrated that electrical trans-membranepotential is correlated to degree of mitotic activity similar structuralalteration could occur in the mitochondrial membrane affecting oxidativephosphorylation.

Normal electrical charge of cell membrane (Steve Haltiwanger's articleon electrical nutrition) is maintained both by normal structure ofmembrane and it's mineral concentration in proper proportion which inturn is required for normal cellular potential & metabolic activity.

Deviations or abnormalities in cancer cells are as follows(Haltiwanger);

Cancerous tissue and less differentiated regenerating tissues are moreelectro negative and cells in these tissues have cell membranes thatexhibit different electrochemical properties and a differentdistribution of electrical charges than normal tissues thereby makingthem less efficient in their production of cellular energy (ATP).

Further cancer cells have altered membrane composition and membranepermeability, which results in the movement of potassium, magnesium andcalcium out of the cell and the accumulation of sodium and water intothe cell, resulting in the cell having have higher intracellular Na+ ionconcentration & lower intra cellular K+, Ca+, and Mg+ ion concentration.This higher intracellular concentration of sodium ions maintain TMP atmuch lower level, leading to carcinogenesis as also causing them to bemore spherical & have different geometry than normal cells and thisswelling in turn leads to disruption in the normal signaling of thecell.

Cancer cells also have different lipid and sterol content than normalcells.

When injury occurs in the body, normal cells proliferate and replace thedamaged or destroyed cells with new cells or scar tissue. Thecharacteristic feature of proliferating cells or cancer cells is thattheir TMP is lower than normal cells (Cone 1975). After the repair iscompleted, the cells stop proliferating and their TMP returns to normaldue to contact inhibition with other cells and this proliferation ofcells is organized.

While in cancer cells, the contact inhibition does not exist due todisrupted electrical connection between cells and their TMP ismaintained at lower level than normal healthy cells. Cancer cells becomeindependent of normal cell signal thereby have desynchronized anddisorganized growth.

ATP is manufactured as a result of several cell processes includingfermentation, respiration and photosynthesis. Most commonly the cellsuse ADP as a precursor molecule and then add a phosphorus to it. Ineukaryotes this can occur either in the soluble portion of the cytoplasm(cytosol) or in special energy-producing structures called mitochondria.Charging ADP to form ATP in the mitochondria is called chemiosmoticphosphorylation. This process occurs in specially constructed chamberslocated in the mitochondrion's inner membranes.

The mitochondrion itself functions to produce an electrical chemicalgradient—somewhat like a battery—by accumulating hydrogen ions in thespace between the inner and outer membrane. This energy comes from theestimated 10,000 enzyme chains in the membranous sacks on themitochondrial walls. Most of the food energy for most organisms isproduced by the electron transport chain. Cellular oxidation in theKrebs cycle causes an electron build-up that is used to push H+ ionsoutward across the inner mitochondrial membrane.

As the charge builds up, it provides an electrical potential thatreleases its energy by causing a flow of hydrogen ions across the innermembrane into the inner chamber. The energy causes an enzyme to beattached to ADP which catalyzes the addition of a third phosphorus toform ATP. Plants can also produce ATP in this manner in theirmitochondria but plants can also produce ATP by using the energy ofsunlight in chloroplasts as discussed later. In the case of eukaryoticanimals the energy comes from food which is converted to pyruvate andthen to acetyl coenzyme A (acetyl CoA). Acetyl CoA then enters the Krebscycle which releases energy that results in the conversion of ADP backinto ATP.

The more protons there are in an area, the more they repel each other.When the repulsion reaches a certain level, the hydrogen ions are forcedout of a revolving-door-like structure mounted on the inner mitochondriamembrane called ATP synthase complexes. This enzyme functions toreattach the phosphates to the ADP molecules, again forming ATP.

The ATP synthase revolving door resembles a molecular water wheel thatharnesses the flow of hydrogen ions in order to build ATP molecules.Each revolution of the wheel requires the energy of about nine hydrogenions returning into the mitochondrial inner chamber. Located on the ATPsynthase are three active sites, each of which converts ADP to ATP withevery turn of the wheel. Under maximum conditions, the ATP synthasewheel turns at a rate of up to 200 revolutions per second, producing 600ATPs during that second.

ATP is used in conjunction with enzymes to cause certain molecules tobond together. The correct molecule first docks in the active site ofthe enzyme along with an ATP molecule. The enzyme then catalyzes thetransfer of one of the ATP phosphates to the molecule, therebytransferring to that molecule the energy stored in the ATP molecule.Next a second molecule docks nearby at a second active site on theenzyme. The phosphate is then transferred to it, providing the energyneeded to bond the two molecules now attached to the enzyme. Once theyare bonded, the new molecule is released. This operation is similar tousing a mechanical jig to properly position two pieces of metal whichare then welded together. Once welded, they are released as a unit andthe process then can begin again.

Apoptosis; Santi Tofani, et al demonstrated that electro-magnetic fieldscause anti-tumor activity and significant increase in apoptosis intumors of treated animals together with reduction in immuno-reactive p53expression. Xiaoqi Liu, found that an overabundance of the polo-likekinase 1, or P1k1, molecule during cell growth, as well as a shortage ofthe p53 molecule, will lead to tumor formation. Studies in Liu'slaboratory showed that the P1k1 molecule indirectly attacks p53 in aprocess called ubiquitination which provides the mechanism for how p53loses its function in cancer cells. The tumor-suppressor protein p53accumulates when DNA is damaged due to a chain of biochemical reactions.Part of this pathway includes alpha-interferon and beta-interferon,which induce transcription of the p53 gene and result in the increase ofp53 protein level and enhancement of cancer cell-apoptosis. p53 preventsthe cell from replicating by stopping the cell cycle at G1, orinterphase, to give the cell time to repair, however it will induceapoptosis if damage is extensive and repair efforts fail. Any disruptionto the regulation of the p53 or interferon genes will result in impairedapoptosis and the possible formation of tumors.

The tumor-suppressor protein p53 accumulates when DNA is damaged due toa chain of biochemical reactions. Part of this pathway includesalpha-interferon and beta-interferon, which induce transcription of thep53 gene and result in the increase of p53 protein level and enhancementof cancer cell-apoptosis. p53 prevents the cell from replicating bystopping the cell cycle at G1, or interphase, to give the cell time torepair, however it will induce apoptosis if damage is extensive andrepair efforts fail. Any disruption to the regulation of the p53 orinterferon genes will result in impaired apoptosis and the possibleformation of tumors.

The tumor-suppressor protein p53 accumulates when DNA is damaged due toa chain of biochemical reactions. Part of this pathway includesalpha-interferon and beta-interferon, which induce transcription of thep53 gene and result in the increase of p53 protein level and enhancementof cancer cell-apoptosis. p53 prevents the cell from replicating bystopping the cell cycle at G1, or interphase, to give the cell time torepair, however it will induce apoptosis if damage is extensive andrepair efforts fail. Any disruption to the regulation of the p53 orinterferon genes will result in impaired apoptosis and the possibleformation of tumors.

The process of apoptosis is controlled by a diverse range of cellsignals, which may originate either extracellular (extrinsic inducers)or intracellular (intrinsic inducers). Extracellular signals may includetoxins, hormones, growth factors, nitric oxide or cytokines, andtherefore must either cross the plasma membrane or transduce to effect aresponse. These signals may positively (i.e., trigger) or negatively(i.e., repress, inhibit, or dampen) affect apoptosis. (Binding andsubsequent initiation of apoptosis by a molecule is termed positiveinduction, whereas the active repression or inhibition of apoptosis by amolecule is termed negative induction.)

A cell initiates intracellular apoptotic signaling in response to astress, which may bring about cell suicide. The binding of nuclearreceptors by glucocorticoids, heat, radiation, nutrient deprivation,viral infection, hypoxia and increased intracellular calciumconcentration, for example, by damage to the membrane, can all triggerthe release of intracellular apoptotic signals by a damaged cell. Anumber of cellular components, such as poly ADP ribose polymerase, mayalso help regulate apoptosis.

Before the actual process of cell death is precipitated by enzymes,apoptotic signals must cause regulatory proteins to initiate theapoptosis pathway. This step allows apoptotic signals to cause celldeath, or the process to be stopped, should the cell no longer need todie. Several proteins are involved, but two main methods of regulationhave been identified: targeting mitochondria functionality, or directlytransduction of the signal via adaptor proteins to the apoptoticmechanisms. Another extrinsic pathway for initiation identified inseveral toxin studies is an increase in calcium concentration within acell caused by drug activity, which also can cause apoptosis via calciumbinding protease calpain.

Many pathways and signals lead to apoptosis, but there is only onemechanism that actually causes the death of a cell. After a cellreceives stimulus, it undergoes organized degradation of cellularorganelles by activated proteolytic caspases. The characteristic changesof a cell undergoing Apoptosis start with the breakdown of theproteinaceous cytoskeleton by caspases causing cell shrinkage androunding, the cytoplasm appears dense and the organelle tightly packedthe process of pyknosis starts with chromatin undergoing condensationwhich is a hallmark of Apoptosis. Further the nuclear envelope becomesdiscontinuous and the process of Karyorrhexis (DNA fragmentation). Atthis time the cell membrane forms irregular blebs and starts to breakapart into vesicles called apoptotic bodies which are then phagocytosed.

Apoptosis progresses quickly and its products are quickly removed,making it difficult to detect or visualize. During karyorrhexis,endonuclease activation leaves short DNA fragments, regularly spaced insize. These give a characteristic “laddered” appearance on agar gelafter electrophoresis. Tests for DNA laddering differentiate apoptosisfrom ischemic or toxic cell death.

The removal of dead cells by neighboring phagocytic cells has beentermed efferocytosis. Dying cells that undergo the final stages ofapoptosis display phagocytotic molecules, such as phosphatidylserine, ontheir cell surface. Phosphatidylserine is normally found on thecytosolic surface of the plasma membrane, but is redistributed duringapoptosis to the extracellular surface by a hypothetical protein knownas scramblase. These molecules mark the cell for phagocytosis by cellspossessing the appropriate receptors, such as macrophages. Uponrecognition, the phagocyte reorganizes its cytoskeleton for engulfmentof the cell. The removal of dying cells by phagocytes occurs in anorderly manner without eliciting an inflammatory response.

Role of Centrioles:

Centrioles are among the simplest structures within the eukaryotic cell,but they play a surprisingly complex set of roles. They are composed ofnine parallel protein rods, which form ribbed, hollow tubes with morethan a passing resemblance to microscopic rigatoni. In pairs, centriolesform the heart of the centrosome, which hovers near the nucleus andcoordinates chromosome division during mitosis. Singly, and docked tothe plasma membrane, they dictate the position and growth of fl agellaand cilia, the hair-like extensions whose coordinated beatings caneither move the cell through liquid or move liquid across the cell'ssurface. They replicate themselves by a templating process, without anydirect instruction from the cell's nucleus. Marshall, Wallace F, 2007.

Centrioles play a role in inheritance of tumorigenic properties whichcontain differently encoded RNA sequences stacked in a definite order.During mitosis, these RNA sequences are released in a pattern thatpossibly cause changes in the status of repressed and potentially activegenes thereby affecting the morphogenetic status of a cell. In eachmitotic division, one of the RNA sequences is released and ‘lost’ so thecentrioles of daughter cells contain one RNA sequence less than thecentrioles of the maternal cell. The number of RNA sequences containedin centrioles decreases after each mitotic division. The last RNAsequence triggers the processes of programmed death (i.e. apoptosis).Thus, the number of sequences correspond to the number of possiblemitotic divisions, counting down from the cell having the firstorthogenetic status to the last offspring cell having the finalmorphogenetic status the “Hayflick limit”.

Microtubules may be a source of endogenous cellular EMF. We havepresented here a simple model of MT EMF geometry and properties.Endogenous cellular EMF may contribute significantly to the dynamic andspatial organization of cellular processes and structures.

FIG. 13. Modifications to the centriole in the normal cell cycle andmitosis (not to scale: centrioles are about 750 nm in length and 200 nmouter m diameter, much smaller than mitotic spindles). Center: centrioleas two perpendicular cylinders. Clockwise from center (G1, S, and G2occur during “Interphase” which precedes and follows mitosis): in G1phase centriole cylinders separate. In S phase centrioles replicate,each cylinder forming a new perpendicular cylinder via connectingfilamentous proteins. G2 phase: centrioles separate and begin tomigrate. Prophase: centrioles move apart and microtubules form themitotic spindles between the centrioles. Metaphase: mitotic spindlesattach to centromeres/kinetochores on opposite sides of each pairedchromosome (only four of which are shown). Anaphase: paired chromosomesseparate into sister chromatids and are moved by (and move along)mitotic spindles to newly forming daughter cells.

FIG. 13. Abnormal centriole activities in mitosis leading to aneuploidy.As in FIGS. 1 and 2 except that defective centriole replicationcontinues in G2 producing three centrioles which form abnormallydistributed spindles in prophase and abnormal chromosomedistribution/genotypes in metaphase and anaphase. This results inchromosomes mal distributed among three daughter cells.

Centrioles do not directly drive the assembly of the spindle, ratherthey recruit a centrosome which sculpts the inherently self-assemblingspindle into a more precise form, and they then act as structuralreinforcements to allow the spindle pole to resist the forces it meetsduring mitosis. Such functions in mitotic fidelity may help explain thenear-universality of supernumerary centrioles in solid tumor cells[Brinkley and Goepfert, 1998; Doxsey, 2002]. Most tumor cells haveabnormal numbers of centrioles, but if this simply resulted in celldeath, the tumor would not progress.

SPMF Signals Producing Order in Cancer Cells:

SPMF effects the regulation of cell membrane potential and gap junctioninter-cellular communication aberrations thereby impactingcarcinogenesis and neutralizing these effects.

SPMF Therapy targets the basic cellular abnormalities and normalizescellular functions by restoring transmembrane potential, therebynormalizing the disrupted or aberrant intracellular and intercellularconnection, preventing electron efflux which is responsible for absolutedecrease in TMP, restoring gap junction inter cellular communicationwith surrounding normal cells by regulating the passage of Ca+ ions andcAMP.

SPMF further restores the p53 function as cell mitosis is arrested bythe change in orientation of centrioles during cell division whichprevents Cyclin E-dependent reduplication of both centrioles andcentrosomes in a single cell division cycle thereby irreversibly markingthe cell for apoptosis. The SPMF also reduces blood volume density intumor thus decreasing chances of distant metastasis.

Clinical Examples of Cancer Treatment

Since 2009, 31 patients have been treated in a clinical trial. Some ofthe benefits of SPMF treatment include:

Improves quality of life;

Halts Progression of the disease;

Significantly decreases pain;

Cure maybe long lasting and the progress of the disease is halted

Alternative to Radiation Therapy

It is an outpatient treatment

Patient case history for 2 patients treated with SPMF.

Case Summary: 30 year old female Diagnosis—Synovial Sarcoma with Mets inRight lung and Mediastinal Lymph Nodes

Diagnosis—Synovial Sarcoma with Mets in Right lung and Mediastinal LymphNodes;

Presentation—July 2007, progressively increasing swelling in the lowerPost Chest wall;

CT Scan; FIG. 9A

FNAC—24 Aug. 2007, Inconclusive;

Surgery—Excision of soft tissue mass on 7 Sep. 2007, at Sydney,Australia;

Post Op Biopsy—Synovial Sarcoma;

Post op Radiotherapy—25#, Oct. 10, 2007 to Dec. 4, 2007;

Chemotherapy—Ifosphamide and doxorubicin—2#, from Jan. 1, 2008 onwards,stopped because of side effects;

Dec. 25, 2008—PET CT well defined nodule in the apical segment of lowerlobe of right lung, S/O metastases;

Jan. 16, 2009—Surgery-Rt. Lower Lobectomy done;

Post op Biopsy—Rt. Lower lung Nodule—conclusive of metastatic SynovialSarcoma;

July 2009—CT Chest+abdomen-Multiple lobulated Pleural masses and a massin Rt. Perihilar region, the surgical Clips in the Left Lumbar regionand Lower lobe Bronchus in situ;

Mar. 23, 2009—CT chest/abdomen—No evidence of Metastasis;

Jul. 22, 2009—Biopsy of Lung Mass—recurrence of Monoplastic SynovialSarcoma; spindle shaped cells focally +ve for EMA;

Presentation at SBF Healthcare Pvt. Ltd;

Breathlessness on walking;

Puffiness and Tightness of lower half of face and upper chest;

Severe pain in the Rt. lower chest (patient on Fentanyl patch, 50mg+NSAIDS);

Wt. loss 4 kgs in past 2 months;

Reduced appetite and energy levels;

Pre-treatment CT Sep. 19, 2009 FIG. 9B;

Course of treatment at SBF Healthcare;

SPMF Therapy—Sep. 20, 2009 to Oct. 17, 2009;

Mid-treatment CT Oct. 7, 2009; FIG. 9C;

Post-treatment PET/CT Oct. 29, 2009; FIG. 9D;

Post-treatment CT Nov. 5, 2009; FIG. 9E;

Palliative RT for SVC syndrome, 12 Gy/3#—Oct. 19, 2009, Oct. 21, 2009and Oct. 22, 2009;

10 days after QMR therapy, she was off the pain killer;

Breathlessness reduced (Climbed 2 flights of stairs withoutbreathlessness) Wt. stabilized.

FIG. 10; Case Summary; 55 Male Diagnosis—Left Posterior Frontal—GBM (WhoGrade—IV)

Diagnosis—Left Posterior Frontal—GBM (WHO Grade—IV) Onset: 26 Mar. 2007;

Presenting symptoms-seizure;

MRI Brain dated May 21, 2007, films only;

Small dense nodular enhancing lesion in left frontal lobe (6×5×6 cms);

Multiple small chronic lacunar infarcts B/L centrum semiovale, parietallobe & periventricular region;

Given ATT and antiepileptic drugs for 06 months.

Recurrence of symptoms;

MRI Brain dated Dec. 27, 2007: Well defined nodular enhancing region inRight frontal convexity 6×4 cms with perilesional edema and adjoiningMeningial enhancement;

Surgery Left posterior frontal craniotomy with excision of tumor on Oct.1, 2008;

HPR: Diffuse infiltrating astrocytoma Gr-II Improved symptomatically;

Post-op RT-54 Gy/30# dated Mar. 10, 2008 to Apr. 25, 2008;

Recurrence of symptoms—Generalized Seizure and Right Hemipareses inNovember/December 2008;

Second Surgery—Left posterior frontal craniotomy with excision of tumoron Jan. 1, 2009.

HPR: GBM Grade IV dated Jan. 14, 2009. (Reported at National Instituteof Mental health and neurosciences, Bangalore, India.) Symptomaticimprovement with residual right Hemipareses;

Patient presented at SBF Healthcare Pvt. Ltd in March 2009 withcomplaints of Right Hemipareses, pain in both legs and headache;

SPMF Therapy—Apr. 4, 2009 to Jan. 5, 2009 (28 days);

Post SPMF: No headache and leg pain. Muscle power improved in Rightupper and lower limbs;

Pre SPMF MRI: lesion size 2.2×3.8 Cms. FIG. 10A, B, C;

Immediate Post SPMF: Lesion size 2.0×3.5 Cms. FIG. 10D, E, F;

Post SPMF 04 months: lesion size 1.4×1.5 Cms. FIG. 10G, H, I;

Treatment Protocols for Tissue Regeneration—The patient process flowchart for arthritis is illustrated in FIG. 17.

Treatment Protocols for Arthritis a predetermined dose profile ispreformed based on the grade and severity of the arthritis and thepermittivity index. Patients who have early stage arthritis will receivea low sensitizing frequency in the range of 8 Hz to 20 Hz, a stimulatingfrequency in the range of 12 Hz to 40 Hz. Patients who have severearthritis and a high permittivity index will receive a sensitizingfrequency of 10 Hz, and a stimulating frequency up to 40 Hz. as per thetable.

TABLE Sensitizing Stimulating Class Frequency Frequency HighPermittivity Grade - I 8 9 High Permittivity Grade - II 8 10 HighPermittivity Grade - III & 8 11 above Low Permittivity Grade - I 8 10Low Permittivity Grade - II 8 12 Low Permittivity Grade - III & 8 14above

Articular Cartilage Regeneration and Repair

In spite of medical and surgical advances in treatment ofosteoarthritis, outcome is still under debate. This is attributable inlarge part to the intrinsic biology of cartilaginous tissue, whichlimits its capacity to self regenerate. Because cartilage isnon-vascularized and non-innervated, the normal mechanism of tissuerepair involving humoral factors and recruitment of stem/progenitorcells to the site of damage does not apply. Moreover, the low densitywithin cartilaginous tissue reduces the likelihood of local chondrocytecontributing to self-regeneration. Targeted stimulation of endogenousrepair mechanism remains specific goal. Achieving this goal depends onunderstanding of cellular and molecular mechanisms of joint formation,articular cartilage injury and repair.

When hyaline cartilage of the knee is destroyed arthritis generallyfollows. The diffuse articular cartilage damage of degenerative orinflammatory arthritis is not amenable to cartilage repair procedures.There are two main types of injury to articular cartilage. The first isacute and transient, consisting of loss of proteoglycan and othernon-collagenous tissue. Such an injury may occur following abnormaljoint loading or the use of anti-inflammatory drugs. Cartilage generallymakes a complete recovery from this type of injury. The second type ofinjury involves mechanical disruption of the collagen network. Thisresults in significant loss of cells and lesions are generallyirreversible and do not successfully heal. In the progression of OA, atan undefined time point, a transition is made from the first to thesecond type of injury.

Although repair of superficial defects in articular cartilage can becomplete for fetal tissues, the same is not true for adult cartilage.There are several reasons why adult chondral defects do not adequatelyheal. First, the anti-adhesive nature of the cartilage matrix preventsstem cells migrating from neighboring synovium to adhere onto thecartilage surface. Second, there is insufficient chemotactic signal fromthe site of injury, as the endogenous chondrocyte population is toosparse. The amount of cytokines and growth factor released is too small.Additionally, despite attempts by endogenous chondrocytes adjacent tothe cartilaginous effect to proliferate and migrate into the defect,they are sterically hindered in doing so by the collagenous matrix ofarticular cartilage. The chondrocytes have only a limited anabolicpotential and are ill-equipped to deal with large tissue failures.

Causes of pain in osteoarthritis of Knee:

1. Synovial membrane inflammation

2. Microfractures of subchondral bone

3. Venous congestion of intraosseous space

4. Joint distention

5. Changed mechanical alignment

6. Bursal inflammation

7. Periosteal stretching due osteophytes

8. Depression

SPMF Therapy in Osteoarthritis:

RPMF Therapy addresses all the above-mentioned abnormalities and causesthe re-generation of cartilage and pain relief in patients ofosteoarthritis; In Osteoarthritis cartilage, there is loss of collagenand proteoglycans preventing generation of piezoelectric stimulus orfailure of this stimulus to stimulate the chondrocytes. Exposure ofcartilage cells to SPMF re-creates the physiological piezoelectricstimulus. Centrioles are cylindrical structures, usually in pairsoriented at right angles to one another. The wall of each centriolecylinder is made of nine interconnected triplet microtubules, arrangedas a pinwheel. The centro somal cycle is closely integrated with thechromosomal cycle in embryonic and somatic cells. In essence, itcontrols the cell cycle and cell division in most cells. Likechromosomes, centrioles are self-replicating organelles, which duplicateduring inter-phase, when they are located close to the nucleus.

In humans, centrioles are formed in the fetal cartilage, but theydisappear during adult life. They have been demonstrated to reappearduring the regenerative process. Exposure of cartilage cells inosteoarthritis patients to specific regulated SPMF therapy fields leadsto denovo-synthesis of centrioles from the microtubules and the proteinsurrounding them, leading to regeneration of cartilage cells.

Insulin-like growth factor-1 (IGF-1) is one of several growth factorsthat have been shown to have an anabolic effect on cartilage growth anddifferentiation. IGF-1 in synovial fluid (SF) is the main stimulatoryfactor responsible for PG synthesis by chondrocytes. There is evidencethat IGF-1 insufficiency plays an etiologic role in OA. In OA cartilagethere is enhanced expression of IGF-1 mRNA as chondrocytes attempt torepair damaged tissue. However, there is also a parallel, greaterdecrease in the responsiveness of chondrocytes to IGF-1. This is in partdue to aging and in part due to the presence of inflammatory cytokines(i.e. IL-1). The net result is diminished anabolic potential for OAcartilage. SPMF Exposure increases the production of IGF-1, which mayplay an important role in facilitating chondrocyte adhesion andproliferation. SPMF Exposure also increases sulphate incorporationrequired for proteoglycan synthesis. SPMF exposure of cells up-regulatesthe HSR/HSF-1 pathway, delay cellular damage & stimulates the naturalstress response and activates the repair process. Delaying thesenescence of cells, the target would be heat shock protein axis, whichis regulated by HSF-1. This pathway (HSP) is preferred to preventprotein damage. In Osteoarthritis cartilage, the chondrocytes havelimited capacities to migrate to the cartilage defects and proliferate.SPMF Exposure of cells increases the synthesis of proteoglycans therebyfacilitating migration of chondrocytes for healing the cartilagedefects.

Relief of pain after few SPMF exposure is brought about by reduction insynovial inflammation that is due to reduction in gap junction mediatedsecretion of pro-inflammatory cytokines. SPMF beam stimulates theproduction opioid peptides activates mast cell and increase the electriccapacity of muscular fibers. SPMF lowers the threshold of nociceptiveafferents innervating the joint capsule, induced by arthritis.

Clinical Outcomes Osteoarthritis

Since 2009, treated over 150 patients in a commercialized model

Range of Motion (ROM) increased progressively in every patient

Total Functional Scores (TFS) and Total Knee Score (TKS) has improved inall patients, who were able to walk comfortably for considerabledistances at the end of the treatment

There was a significant increase in the cartilage thickness after SPMFtherapy

Improves stability and power of the knee joint

Progress of the disease is halted

Significantly decreases pain

Cure is long lasting and the progress of the disease is halted

Enables natural growth of cartilage and increases its thickness asagainst placement of foreign substance

Alternative to knee replacement

Both knees can be treated simultaneously

It is an outpatient treatment

Patients can carry on their normal activity during the treatment

Patient case history;

FIGS. 11A, B, C, D, Case Summary; Osteo Arthritis

SPMF Treatment was performed for 21 days;

After 90 days of treatment the total knee score (TKS) increased from 55to 80 illustrated in FIG. 11 a, and the cartilage thickness increasedfrom 0.05 mm to 0.06 mm illustrated in FIG. 11 b,c,d;

Progress Report for SPMF Therapy, FIG. 1 a;

MRI Image of the left knee Pre SPMF Therapy FIG. 11 b;

MRI Image of right knee Pre SPMF Therapy FIG. 11 c;

MRI Images of both knees Post SPMF Therapy MRI Images FIG. 11 d;

Treatment Protocols for Neural Disorders & NeurodegenerativeDiseases—The patient process flow chart for neuro is illustrated in FIG.18.

Neuro degeneration, the progressive loss of nerve cells, occurs in agingand in neurodegenerative disorders, such as Alzheimer's, Parkinson's,ALS, and Huntington's disease, in retinal degeneration, and other damageto sensory systems (e.g., visual, auditory, somatosensory), in stroke,head and spinal trauma, epilepsy, in drug and alcohol abuse, ininfectious diseases, in exposure to industrial and environmentaltoxicants, and, perhaps, in mental disorders and chronic pain.Primarily, these diseases are characterized by chronic and progressiveloss of neurons in discrete areas of the brain, causing debilitatingsymptoms such as dementia, loss of memory, loss of sensory or motorcapability, decreased overall quality of life and well-being,disability, and eventually, premature death.

Classification:

Neurodegenerative diseases are crudely divided into two groups accordingto phenotypic effects, although these are not mutually exclusive:Conditions causing problems with movements, such as ataxia, andConditions affecting memory and related to dementia

List of neurodegenerative diseases and conditions:

Adrenoleukodystrophy (ALD), Alcoholism, Alexander's disease, Alper'sdisease, Alzheimer's disease, Amyotrophic lateral sclerosis (LouGehrig's Disease), Ataxia telangiectasia, Batten disease (also known asSpielmeyer-Vogt-Sjögren-Batten disease), Bovine spongiformencephalopathy (BSE), Canavan disease, Cockayne syndrome, Corticobasaldegeneration, Creutzfeldt-Jakob disease, Familial fatal insomnia,Frontotemporal lobar degeneration, Huntington's disease, HIV-associateddementia, Kennedy's disease, Krabbe's disease, Lewy body dementia,Neuroborreliosis, Machado-Joseph disease (Spinocerebellar ataxia type3), Macular Degeneration, Multiple System Atrophy, Multiple sclerosis,Narcolepsy, Niemann Pick disease, Parkinson's disease,Pelizaeus-Merzbacher Disease, Pick's disease, Primary lateral sclerosis,Prion diseases, Progressive Supranuclear Palsy, Refsum's disease,Sandhoff disease, Schilder's disease, Subacute combined degeneration ofspinal cord secondary to Pernicious Anaemia,Spielmeyer-Vogt-Sjogren-Batten disease (also known as Batten disease),Spinocerebellar ataxia (multiple types with varying characteristics),Spinal muscular atrophy, Steele-Richardson-Olszewski disease, Tabesdorsalis, Toxic encephalopathy, Path physiology and others.

Neuro degeneration is often caused by mis folding of proteins (prions)in such way that they can no longer perform their cellular functions andinstead triggers equivalent modifications in normal proteins, thuscreating a cascade of damage that eventually results in significantneuronal death. In humans, this can cause Creutzfeldt-Jakob disease orvariant CJD (Mad Cow Disease).

Normally, neuro degeneration begins long before the patient experiencesany symptoms. It can be months or years before any effect is felt.Symptoms are noticed when many cells die or cease to function.

Additionally, the role of microglia in modulating neuro inflammation inCNS-related degeneration is currently being studied.

Treatment:

For most neurodegenerative diseases, there is little or no treatment; atbest, treatments are symptomatic in nature and do not prevent or slowthe progression of disease. Clearly, an understanding of pathologicalprogression can help to identify points of intervention and lead topromising therapeutic approaches. A fundamental approach for reducingthe burden of neurodegenerative diseases is thus to slow or haltprogression, and ultimately, to prevent the onset of the diseaseprocess. Strategies for neuro rescue, neuro repair, or neuroprotectionare being actively pursued by the basic, translational, and clinicalresearch communities. As our population ages, the already enormousimpact of neuro degeneration on society will become even larger withoutbetter prevention and treatment.

Initial treatment for neurodegenerative disorders is dependent ondiagnosis of the underlying condition. Presently, few therapies areavailable for the treatment of most neurodegenerative diseases.Treatment with L-dopa can inhibit symptoms of Parkinson's Disease for ashort time, but is thought to subsequently accelerate the progression ofsymptoms. Efforts are being made to develop therapies for Alzheimer'sDisease in order to stabilize cognitive function.

Epidemiology

Stem cell technology and stem cell treatments, as well as Gene therapyare gaining increasing attention for the treatment of neurodegenerativediseases. Research is underway into biomarkers as part of an attempt tounderstand the progression of certain types of neurodegenerativedisease. In theory, if relevant biomarkers were identified, people couldbe treated for such diseases prior to onset of symptoms, thus resultingin a significant extension of their normal functional lifespan. Yet,however, the science of biomarkers is in its infancy and consequentlydiagnosis of neurodegenerative disease tends to occur after the patienthas already suffered the majority of the neural damages. However, theuse of electromagnetic fields in neural regeneration has been triedearlier with little success. With this method, and the protocols usedthe efficacy of treatment is enhanced as the SPMF can be targeted on thespecific areas (region of interest) using selective algorithms based ontissue type.

The algorithms used in neuro degenerative diseases are as follows:

First, a proton density, MRI of the brain is performed, then the areamapping is carried out based on the algorithm described below, and thenthe dose pattern is mapped out for the patient.

NEURO DEGENERATIVE DISEASES (Range 30-120 Hz) Flow Chart FIG. 18 is aflow chart for patient treatment of neuro MinimumDensity = 3^(rd)minimum of PixelValue MaximumDensity = 3^(rd) Maximum of PixelValueAverageDensity = (Sum of Pixel Values \ No. Of Pixel Values)SkinToTarget = Root((xe−xs){circumflex over ( )}2 +(ye−ys){circumflexover ( )}2 ) Sensitizing frequency= ( X ) = Min density*2 ΠCon_Sen_Freq= (X) / (Π² * e) e ≈ 2.718 (Euler's constant) If Sensitizingfreq >= 60 Then Sensitizing freq = 60 Else If Sensitizing freq <= 30Then Sensitizing freq = 30 6) DownloadPul Sensitizing =HEX(65536-(500000/ Sensitizing freq)) 7) Stimulating Frequency = Y =Max density * (Π/2)Con_sti_freq= ( Y ) / ( Π² ) If Stimulating Freq >= 120 Then StimulatingFreq =120 ELSE If Stimulating Freq <= 80 Then Stimulating Freq = 808)DownloadPul Stimulating =HEX(65536-(500000 / Stimulating Freq)) 9)k =Π * e e ≈ 2.718 (Euler's constant) 10)Pulse Cnt Sensitizing =Sensitizing freq / k 11)Pulse Cnt Stimulating = Stimulating freq / k

Clinical Data examined—Patient Dr. C aged 60 years patient ofSpinocerebellar Ataxia 1 came with significant speech defects ataxia andhence has difficulty in walking since 2 years was unable to walk on asmooth surface without support and had episodes of frequent fall and shewas unable to go to her clinic and continue her clinical practice. Shewas treated with SPMF therapy for 4 weeks after which she startedshowing improvement gradually and the next 3 months, her speech and gaitimproved to an extent that she could walk independently and she could goback to seeing patients in her clinic and in 6 months, she had almostreached normalcy.

Ménière's disease is an abnormality of the inner ear causing a host ofsymptoms, including vertigo or severe dizziness, tinnitus or a roaringsound in the ears, fluctuating hearing loss, and the sensation ofpressure or pain in the affected ear. The disorder usually affects onlyone ear and is a common cause of hearing loss. Named after Frenchphysician Prosper Ménière who first described the syndrome in 1861.

The symptoms of Ménière's disease are associated with a change in fluidvolume within a portion of the inner ear known as the labyrinth. Thelabyrinth has two parts: the bony labyrinth and the membranouslabyrinth. The membranous labyrinth, which is encased by bone, isnecessary for hearing and balance and is filled with a fluid calledendolymph. When your head moves, endolymph moves, causing nervereceptors in the membranous labyrinth to send signals to the brain aboutthe body's motion. An increase in endolymph, however, can cause themembranous labyrinth to balloon or dilate, a condition known asendolymphatic hydrops.

Many experts on Ménière's disease think that a rupture of the membranouslabyrinth allows the endolymph to mix with perilymph, another inner earfluid that occupies the space between the membranous labyrinth and thebony inner ear. This mixing, scientists believe, can cause the symptomsof Ménière's disease. Scientists are investigating several possiblecauses of the disease, including environmental factors, such as noisepollution and viral infections, as well as biological factors.

Symptoms:

The symptoms of Ménière's disease occur suddenly and can arise daily oras infrequently as once a year. Vertigo, often the most debilitatingsymptom of Ménière's disease, typically involves a whirling dizzinessthat forces the sufferer to lie down. Vertigo attacks can lead to severenausea, vomiting, and sweating and often come with little or no warning.

Some individuals with Ménière's disease have attacks that start withtinnitus (ear noises), a loss of hearing, or a full feeling or pressurein the affected ear. It is important to remember that all of thesesymptoms are unpredictable. Typically, the attack is characterized by acombination of vertigo, tinnitus, and hearing loss lasting severalhours. People experience these discomforts at varying frequencies,durations, and intensities. Some may feel slight vertigo a few times ayear. Others may be occasionally disturbed by intense, uncontrollabletinnitus while sleeping. Ménière's disease sufferers may also notice ahearing loss and feel unsteady all day long for prolonged periods. Otheroccasional symptoms of Ménière's disease include headaches, abdominaldiscomfort, and diarrhea. A person's hearing tends to recover betweenattacks but over time becomes worse. There was no cure for Ménière'sdisease.

MENIERES DISEASE (Range 8-30 Hz) MinimumDensity = 3rd minimum ofPixelValue MaximumDensity = 3rd Maximum of PixelValue AverageDensity =(SumofPixelValues \ No. Of PixelValues) SkinToTarget =Root((xe−xs){circumflex over ( )}2 +(ye−ys){circumflex over ( )}2 )Sensitizing frequency= ( X ) = Min density*2 Π Con_Sen_Freq= (x) / (4 *Π) If Sensitizing freq >= 10 Then Sensitizing freq = 10 Else IfSensitizing freq <= 8 Then Sensitizing freq = 8 6) Download PulSensitizing =HEX (65536-(500000 / Sensitizing freq)) 7) StimulatingFrequency = (y) = Max density * (Π/2) Con_Sti_Freq= (y) / (4 * Π) IfStimulating Freq >= 30 Then Stimulating Freq = 30 8)DownloadPulStimulating =HEX(65536-(500000 / Stimulating Freq)) 9)k = (maxd * mind)/ (“AvgDensity”) 10)PulseCnt Sensitizing = Sensitizing freq / k pcntSensitizing =4 /* Constant Value */ 11)PulseCnt Stimulating =Stimulating freq / k If pcnt Stimulating <= 4 Then pcnt Stimulating = 4Else If pcnt Stimulating >= 14 Then pcnt Stimulating = 14

Macular Degeneration (Degeneration of tissue) (medical condition usuallyof older adults that results in a loss of vision in the center of thevisual field (the macula) because of damage to the retina)

Clinical Outcomes

Non-invasive procedure for treatment.

Significantly decreases pain.

No side effects.

Cure is long lasting and the progress of the disease is halted.

Enables natural growth of cells

It is an outpatient treatment.

Patients can carry on their normal activity during the treatment.

Although the invention has been described with reference to exemplaryembodiments, it is not limited thereto. Those skilled in the art willappreciate that numerous changes and modifications may be made to thepreferred embodiments of the invention and that such changes andmodifications may be made without departing from the true spirit of theinvention. It is therefore intended that the appended claims cover beconstrued to all such equivalent variations as fall within the truespirit and scope of the invention.

1. An apparatus for generating and applying a sequentially programmedmagnetic field to a desired tissue comprising: a plurality of magneticfield generators to produce sequentially programmed pulsed magneticfields at a focal region; and a switching system to control the pulsingin a range of about 0.1 Hz to about 2000 Hz dependent on the diseasetype and the treatment to be administered.
 2. The apparatus of claim 1,further comprising: a tubular gantry for housing the magnetic fieldgenerators, wherein the magnetic field generators are fixedcircumferentially on a tubular gantry in regular intervals of about 15to about 90 degrees with respect to an adjacent magnetic fieldgenerators with reference to the central axis of said tubular gantry. 3.The apparatus of claim 2, wherein: the plurality of magnetic fieldgenerators are operatively coupled in mated, opposed pairs, such thatpairs of magnetic field generators which are about 180 degrees oppositeto each other in said tubular gantry are energized at the same time andout of phase so that the net magnetic flux passes through the focalpoint.
 4. The apparatus of claim 1, further comprising: a tubulargantry, defining from 1 to 12 transverse planes with respect to thecentral axis of said gantry along which said plurality of magnetic fieldgenerators are located; in each transverse plane, 2-24 magnetic fieldgenerators are disposed radially over the circumference of the gantry;and diametrically opposite magnetic field generators are operativelycoupled to form 1 to 12 such pairs wherein each of the pairs can beexcited to generate a magnetic field.
 5. The apparatus of claim 4,wherein circumferentially adjacent magnetic field generators aredisplaced from each other by regular intervals of about 15 to about 180degrees.
 6. The magnetic field generating device of claim 1, furthercomprising: a computer coupled to and controlling the magnetic fieldgenerators, wherein the computer controls the magnetic field generatorsbased on the disease type; computer software stored on the computer forcalculating the duration of the exposure, the pulse frequency, and thefrequency of the firing depending on the patient and the disease type.7. A magnetic field generating device comprising: a magneticallyconductive hollow cylindrical base body extending at one end into afunnel; a magnetically conductive rod-like structure extending throughsaid hollow cylindrical base body into said funnel; and an electricalcoil wound around the hollow cylindrical base body and the funnel. 8.The magnetic field generating device of claim 7, wherein said rod-likestructure defines a frusto-conical end which extends into said funnel.9. The magnetic field generating device of claim 7, further comprisingan external magnetic shield limiting leakage of magnetism except throughsaid funnel.
 10. The magnetic field generating device of claim 7 havingan impedance of from about 80 to about 90 ohms.
 11. A method forinducing cellular regeneration and/or degeneration in a patient in needthereof comprising: applying a programmed pulsed magnetic field to adesired tissue in a sequential pattern.
 12. The method of claim 11,wherein said programmed pulsed magnetic field is generated and appliedin accordance with a treatment plan, said method further comprising:identifying a region of interest; obtaining a specific proton densitythrough the approximate center of the region of interest; determiningoperating parameters selected from sensitizing frequency, stimulatingfrequency, sensitizing pulse count, and stimulating pulse count based ondisease type, the proton density and the duration of exposure at theregion of interest.
 13. The method of claim 12, wherein said operatingparameters selected from sensitizing frequency, stimulating frequency,sensitizing pulse count, and stimulating pulse count are determined as afunction of minimum density, maximum density, average density, which arebased on signal intensity, skin to target intensities and distancewherein the specific proton density is represented by an image, signalintensity is measured over time at any given pixel in the proton densityimage; minimum density is the third lowest signal intensity at a givenpixel in the proton density image; maximum density is the third highestsignal intensity at another given pixel in the proton density image; andaverage density is the sum of pixel values divided by the number ofpixel values; and the Skin to Target value is derived by the root valueof xe (x axis target)−xs (x axis Skin) squared plus ye (y axistarget)−ys(y axis skin) squared.
 14. The method of claim 11, whereinsaid sequential pattern is substantially rotary.
 15. The method of claim14, further comprising: generating said pulsed magnetic field using aplurality of mated and opposed pairs of magnetic field generators; andsimultaneously firing out of phase the mated and opposed pair, whereineach mated and opposed pair is fired in a sequential, substantiallyrotary pattern.
 16. The method of claim 15, further comprising:energizing the mated and opposed pairs of magnetic field generators inthe rotary pattern to focus the net magnetic flux generated by the matedand opposed pairs of magnetic field generators at a focal point oftissue to be treated in the patient.
 17. The method of claim 15, furthercomprising: aligning the area to be treated at the focal point;generating the pulsed magnetic field at a predetermined pulsingfrequency in the range of about 0.1 Hz to about 2000 Hz dependent on adisease type and treatment to be administered; applying a sensitizingtreatment phase at the focal point for a predetermined durationdependent on the disease type and treatment to be administered; andapplying a stimulating treatment phase at the focal point for apredetermined duration dependent on the disease type and treatment to beadministered.
 18. The method of claim 17, further comprising: planningthe treatment based upon a patient and disease type; calculating theduration of the exposure, the pulse frequency, the frequency of thefiring, and the sequence of the firing based upon the patient anddisease type.
 19. The method of claim 15, further comprising: connectingthe diametrically disposed coils of the paired magnetic field generatorsin series; subjecting the paired magnetic field generators to arectangular pulse operating out of phase with respect to each other toproduce an effective magnetic field at the region of interest; whereinthe pulse characteristics are selected from: frequency of about 0.1 Hzto about 2000 Hz; pulse count of about 2 to about 50; current of about0.1 amps to about 5 amps; voltage from about 20 V to about 65 V;producing effective magnetic field of about 0.01 to about 5 mT; whereinthe time duration between the switching off and the switching on of theadjacent pair diametrically disposed magnetic field generators is about1 msec to about 5 msec.
 20. A method for treating cancer in a patient inneed thereof, comprising applying a programmed pulsed magnetic field toa desired tissue in a sequential pattern, wherein the pulsingfrequencies are in the range of about 120 Hz to about 2000 Hz.
 21. Themethod of claim 20, wherein the step of applying the pulsed magneticfield further comprises: applying a sensitizing treatment phase at afrequency range of about 0.1 Hz to about 600 Hz; and then applying astimulating treatment phase a frequency range of about 600 Hz to about2000 Hz.
 22. The method of claim 21, wherein the treatment isadministered for a predetermined duration and interval of about 1 hourper day for about 28 days.
 23. The method of claim 20, wherein saidpulsed magnetic field is generated and applied in accordance with atreatment plan, said method further comprising: identifying a region ofinterest; obtaining a specific proton density through the approximatecenter of the region of interest; determining operating parametersselected from sensitizing frequency, stimulating frequency, sensitizingpulse count, and stimulating pulse count based on disease type, theduration of exposure and the proton density image.
 24. The method ofclaim 23, wherein said operating parameters selected from sensitizingfrequency, stimulating frequency, sensitizing pulse count, andstimulating pulse count are determined as a function of minimum density,maximum density, average density, which are based on signal intensity,skin to target intensities and distance, wherein the specific protondensity is represented by an image; signal intensity is measured overtime at any given pixel in the proton density image; minimum density isthe third lowest signal intensity at a given pixel in the proton densityimage; maximum density is the third highest signal intensity at anothergiven pixel in the proton density image; and average density is the sumof pixel values divided by the number of pixel values; and the Skin toTarget value is derived by the root value of xe (x axis target)−xs (xaxis Skin) squared plus ye (y axis target)−ys(y axis skin) squared. 25.The method of claim 24, wherein the region of interest has high protondensity, further comprising the step of calculating sensitizingfrequency=minimum density*2 π; stimulating frequency=maximumdensity*π/2; sensitizing pulse count=the sensitizing frequency/(maximumdensity*minimum density/average density); and stimulating pulsecount=the stimulating frequency/(maximum density*minimum density/averagedensity).
 26. The method of claim 24, wherein the region of interest haslow proton density, further comprising the step of calculating:sensitizing frequency=average density*π; stimulating frequency=maximumdensity*π; sensitizing pulse count=the sensitizing frequency/(thestimulating frequency*the stimulating pulse count); and stimulatingpulse count=the stimulating frequency/((Maximum Density*MinimumDensity)/(Average Density times π²)), provided that when the stimulatingpulse count is less than 10, the stimulating pulse count is set at 10,and that when the stimulating pulse count is greater than 50, thestimulating pulse count is set at
 50. 27. A method for treatingarthritis in a patient in need thereof, comprising applying a pulsedmagnetic field to a desired tissue in a sequential pattern, wherein thepulsing frequencies are in the range of about 8 Hz to about 50 Hz. 28.The method of claim 27, wherein the step of applying the pulsed magneticfield further comprises: applying a sensitizing treatment phase at afrequency range of about 8 Hz to about 20 Hz; and then applying astimulating treatment phase a frequency range of about 12 Hz to about 40Hz.
 29. The method of claim 27, wherein the treatment is administeredfor a predetermined duration and interval of about 45 minutes to about 1hour per day for about 21 days.
 30. A method for treatingneurodegenerative disorders in a patient in need thereof, comprisingapplying a pulsed magnetic field to a desired tissue in a sequentialpattern, wherein the pulsing frequencies are in the range of about 30 Hzto about 120 Hz.
 31. The method of claim 30, wherein the step ofapplying the pulsed magnetic field further comprises: applying asensitizing treatment phase at a frequency range of about 30 Hz to about60 Hz; and then applying a stimulating treatment phase a frequency rangeof about 90 Hz to about 120 Hz.
 32. The method of claim 30, wherein thetreatment is administered for a predetermined duration and interval ofabout 1 hour per day for about 21 days.
 33. The method of claim 30,wherein the neurodegenerative disorder is selected from Alzheimer's,Parkinson's, ALS, and Huntington's disease, in retinal degeneration, andother damage to sensory systems associated with stroke, head and spinaltrauma, epilepsy, drug and alcohol abuse, infectious diseases, mentaldisorders, or from exposure to industrial and environmental toxicants,and chronic pain.
 34. The method of claim 30, wherein said pulsedmagnetic field is generated and applied in accordance with a treatmentplan, said method further comprising: identifying a region of interest;obtaining a specific proton density through the approximate center ofthe region of interest; determining operating parameters selected fromsensitizing frequency, stimulating frequency, sensitizing pulse count,and stimulating pulse count based on disease type, duration of exposureand the proton density.
 35. The method of claim 34, wherein saidoperating parameters selected from sensitizing frequency, stimulatingfrequency, sensitizing pulse count, and stimulating pulse count aredetermined as a function of minimum density, maximum density, averagedensity, which are based on signal intensity, skin to target intensitiesand distance, wherein the specific proton density is represented by animage; signal intensity is measured over time at any given pixel in theproton density image; minimum density is the third lowest signalintensity at a given pixel in the proton density image; maximum densityis the third highest signal intensity at another given pixel in theproton density image; and average density is the sum of pixel valuesdivided by the number of pixel values; and the Skin to Target value isderived by the root value of xe (x axis target)−xs (x axis Skin) squaredplus ye (y axis target)−ys(y axis skin) squared.
 36. The method of claim35, wherein the region of interest has high proton density, furthercomprising the step of calculating sensitizing frequency=minimumdensity*2π, provided that when the calculated sensitizing frequency isless than 30 Hz, the sensitizing frequency is set at 30 Hz and when thecalculated sensitizing frequency is greater than 60 Hz, the sensitizingfrequency is set at 60 Hz. stimulating frequency=Max density*(π/2),provided that when the calculated stimulating frequency is less than 80Hz, the stimulating frequency is set at 80 Hz, and when the calculatedstimulating frequency is greater than 120 Hz, the stimulating frequencyis set at 120 Hz; sensitizing pulse count=sensitizing frequency/π*e,where e≈2.718 (Euler's constant) and stimulating pulse count=thestimulating frequency/π*e, where e, where e≈2.718 (Euler's constant).37. The method of claim 30, wherein the condition to be treated isMenieres disease, and said pulsed magnetic field is generated andapplied in accordance with a treatment plan, said method furthercomprising: identifying a region of interest; obtaining a specificproton density image through the approximate center of the region ofinterest, which comprises a plurality of pixel values; determiningoperating parameters selected from sensitizing frequency, stimulatingfrequency, sensitizing pulse count, and stimulating pulse count based ondisease type, duration of exposure and the proton density image.
 38. Themethod of claim 37, wherein said operating parameters selected fromsensitizing frequency, stimulating frequency, sensitizing pulse count,and stimulating pulse count are determined as a function of minimumdensity, maximum density, average density, which are based on signalintensity, skin to target intensities and distance, wherein signalintensity is measured over time at a given pixel in the proton densityimage; minimum density is the third lowest signal intensity at a givenpixel in the proton density image; maximum density is the third highestsignal intensity at another given pixel in the proton density image; andaverage density is the sum of pixel values divided by the number ofpixel values; and the Skin to Target value is derived by the root valueof xe (x axis target)−xs (x axis Skin) squared plus ye (y axistarget)−ys(y axis skin) squared.
 39. The method of claim 38, wherein theregion of interest has high proton density, further comprising the stepof calculating sensitizing frequency=minimum density*2π, provided thatwhen the calculated sensitizing frequency is less than 8 Hz, thesensitizing frequency is set at 8 Hz and when the calculated sensitizingfrequency is greater than 10 Hz, the sensitizing frequency is set at 10Hz. stimulating frequency=Max density*(π/2), provided that when thecalculated stimulating frequency is greater than 30 Hz, the stimulatingfrequency is set at 30 Hz; sensitizing pulse count=the sensitizingfrequency/(maximum density*minimum density/average density); andstimulating pulse count=the stimulating frequency/(maximumdensity*minimum density/average density), provided that when thecalculated stimulating pulse count is less than 4, the stimulating pulsecount is set at 4, and when the stimulating pulse count is greater than14, the stimulating pulse count is set at 14.